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206 Cards in this Set
- Front
- Back
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What are the clinical manifestations of classic measles?
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-formation of infected cell syncytia due to cell fusion is characteristic, this allows for direct cell to cell infection
-it is a paramyxovirus -incubation 10-14 days -multiplies in resp. epithelium and LNs -viremia, dissemination to other tissues by monocytes secondary viremia |
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Describe the prodromal stage of measles.
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occurs 1-12 days post infection
-high fever -the 3 C's (coryza, persistent cough, conjunctivitis) -Koplik's spots on buccal mucosa (diagnostic) disappear 2-3 days after rash eruption |
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Describe the rash stage of measles.
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appears 3-4 days after prodrome stage starts
-measles rash begins below ears, spreads over forehead to face, neck, extremities in 3 days -rash often very extensive, lesions may become merged on face and back |
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Describe the resolution stage of measles.
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-rise in ab titers, viremia stops
-rash fades in same order it appears |
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What are the 3 stages of classic measles?
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1)prodrome
2)rash 3)resolution |
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What is atypical measles?
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-occurs in pts who received the formalin-inactivated vaccine who were later exposed to wild type virus or newer gen. vaccines
-this vaccine has now been replaced -sx include unusual rash palms/soles with a centripetal spread -rash spares face -the process of formalin inactivation denatured the viral F protein such that pts did not develop protective anti-F abs and were actually sensitized to virus |
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What are the complications of measles infection?
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1)pneumonia
2)diarrhea 3)immunologic abnormalities 4)CNS involvement-SSPE |
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Describe pneumonia as a complication of measles.
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most frequent life-threatening measles infection complication
-accounts for most measles deaths -malnourished and aged at greatest risk |
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Describe CNS involvement as a complication of measles.
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-acute sx encephalitis
-high fatality -a substantial number of measles pts will have some manifestation of encephalitis (0.5%) -ex: SSPE, now very rare in US but typically fatal, will see slow onset changes in personality, behavior and memory |
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Describe immunologic abnormalities as a complication of measles.
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-occur with acute infection
-virus induced immunosuppression probably contributes to development of complicating secondary infections -altered lymphokine production -decreased production of O2 radicals, PMN chemotaxis, DTH suppression, TB exacerbation |
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What type of virus is measles?
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a paramyxovirus
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Describe the structure of the measles virus.
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(-) sense ssRNA linear non segmented genome
-enveloped -virus expresses proteins F (fusion protein responsible for infection spreading) and H (hemagglutinin needed for attachment) -virus replication occurs in cytoplasm |
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Describe the epidemiology of measles.
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-humans and monkeys are the only known hosts
-infection is almost always symptomatic -no healthy carrier state known/no latent/persistent infections -classic measles primarily a disease of kids who aren't vaccinated -rare in infants <6 mos -endemic throughout the yr in heavily pop. areas -has a 2-3 year epidemic cycle when susceptible kids reach suitable numbers, but disease usually peaks with initiation of drier weather in Spring -infection can only be maintained by an unbroken chain of human infections -transmitted via resp. droplets -highly contagious! -virion survival in inversely proportional to humidity -newborns primary source of new infectables -infects small b.v.'s, resp. tract, CNS, urinary tract -pt communicable during prodrome until 4-5 days after rash erupts (max. during late prodrome when pts. coughing) -virus shedding is greatly prolonged in malnourished/immunocompromised ppl -life long immunity after natural infection, vaccine protection requires booster |
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How is measles diagnosed?
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-primarily on clinical findings
-rash and/or Koplik's spots -MACELISA -serology titer (IgG) -FA test on cells obtained from pharynx, nasal and buccal cavities-multinucleated giant cells, this works even when virus can't be cultured - |
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How is measles prevented?
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-controlled by vaccine and natural infections
-MMR, live attenuated measles virus -12-15 mos first dose/4-6 yrs for second dose or anytime 1 month after 1st dose -2-5% of pop. unprotected after single admin. of vaccine -measles outbreaks linked to import of infection by unvaccinated air travelers-number of cases has reached a 15 yr high!!!! -Vaccine CI: neomycin or egg sensitivity, prego, immunocompromised |
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How is atypical measles prevented?
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no longer a concern with modern MMR vaccine
-these pts received a killed measles virus vaccine that led to pts that were measles sensitized but not protected, then when exposed to wild type virus or given live, atten. vaccine they got sx of atypical measles |
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What is tropical measles?
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-measles has a high level of fatality in tropical countries
-nutritional imbalances such as vit. A defic. increase measles severity -vit A supplementation could reduce measles mortality by up to 50% |
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What is rubella?
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AKA german measles or "little red"
-mild exanthematous disease in kids and adults, devastating effects when occurring in utero -sometimes known as "3rd disease" |
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What are the clinical manifestations of rubella?
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14-21 day incubation period
-minimal prodromal sx/more prominent in older pts. -maculopapular rash appears first on face and spreads downward -resolves in order of appearance much like measles (rubeola) -sometimes confused with scarlet fever -mild fever, malaise, conjunctivitis, coryza, lymphadenopathy |
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Describe the rubella viral agent.
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-togavirus
-respiratory route of infection in contrast to other togaviruses -lack of cytopathic effects -ssRNA + sense, enveloped |
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Describe the epidemiology of rubella.
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-endemic in most large cities
-most prevalent in spring -resp. droplet route of spread -virus released 7 days prior to 14 days following rash -pt is communicable 5 days prior to 5 days after rash appears -close and prolonged contact probably needed for infection -humans are only reservoir -world wide distribution but clinical disease occurs less often in tropics -higher incidence in older kids, adolescents, young adults -children often escape natural infection |
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What are the complications of rubella infection?
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-postnatal rubella death is very rare
-rubella was originally thought to be benign until CRS (congenital rubella syndrome) recognition -CRS is usually severe, maternal infection may lead to placental infection and fetal infection -rubella infection early in prego creates a very substantial risk to fetus (cardiac defects-pulm art stenosis, PDA), eye defects-cataracts, glaucoma, hearing loss, CNS involvement -the timing of rubella infection is critical element in outcome-earlier in prego is worse (first and second month hold the most risk) -vaccination has nearly eliminated CRS in US |
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How is diagnosis of rubella made?
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-very difficult
-detection of ab most commonly used, anti-Rubella IgM 4X increase in titer -viral CPE is typically weak and culture methods are rarely employed for rubella |
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How is rubella treated and prevented?
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-sx relief only
-infants with CRS considered infectious for at least 1 yr -vaccine is available (MMR) but CI during prego -key goal is to avoid infection during 1st trimester of prego -determine immune status of females at all opportunities such as marriage, delivery, prenatally -exclude kids from school for 7 days after rash |
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How is varicella zoster virus unusual for a herpes virus?
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virtually all primary infections have signs and sx
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Describe the varicella zoster virus.
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-it is a herpesvirus (alphavirus)
-the hallmark of all herpesviruses is establishment of permanent latency after primary infection -large, enveloped virus with a capsid -genome is single linear dsDNA -only one serotype but genetic mutations in natural virus pops. have been seen |
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Where in the cell does VZV replication take place?
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-in host cell nucleus
-virus grows rather slowly in tissue culture |
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What are the clinical manifestations of chickenpox?
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-asymmetrical vesicular rash that often follows a dermatomal pattern
-fever, malaise, HA, neuralgia -mortality rates low, but increase with advancing age and prego -lesions are pruritic and often secondarily infected by bacteria -hallmark of this disease is to observe the presence of vesicles in several different stages of development |
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How does the chickenpox virus infect a person (via what route)?
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-infects through conjunctiva or respiratory tract mucosa and has a two-stage viremia
-replicates in regional LNs, primary viremia 4-6 days after infection -virus replicates in liver and spleen generating a secondary viremia (10-14 days after infection) -immunocompromised children at great risk -resp. secretion spread, infection through conjunctiva and resp. mucosa are considered likely but exact mode not known -virus is also present in vesicles -highly contagious -incubation period 15 days |
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Describe the epidemiology of chickenpox.
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-worldwide
-humans are only known reservoir -seasonal occurrence peak in winter/spring -highest incidence in 5-9 age group -pt. most contagious 1-2 days before appearance of lesions and 4-5 days after -prodromal sx in older kids and adults are ABSENT IN YOUNGER KIDS |
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How is the diagnosis of chickenpox made?
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-clinical findings usually sufficient
-rash and fever -presence of multinucleated giant cells and intranuclear inclusions in vesicles |
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What is the tx for chickenpox?
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-no specific therapy
-aspirin not recommended due to Reyes risk -lotions to control itching -passive immunization possible with VZIG up to 3 days post exposure for high risk pts to prevent disease or modify disease course |
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How is chickenpox prevented?
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-vaccine is available (varivax)
-given at 12-18 mos of age by subcutaneous injection -adolescents/adults get 2 admininstrations of vaccine |
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What are some of the concerns about varivax?
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-vaccinated persons are a risk to develop shingles but the risk is substantially lower than in an individual infected with wild-type virus
-breakthrough varicella cases in which vaccination derived immunity wanes are now fairly common but usually mild -breakthrough rates increase with elapsed time after vaccination -it is possible that a decreased rate of chickenpox in kids may increase shingles attacks in adults who have had natural cases of chickenpox |
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What are the complications of chickenpox?
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bacterial superinfection of lesions by GABHS
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Describe shingles.
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-typically a disease of adults caused by recrudescence of VZV
-absolute prerequisite for shingles is prior case of varicella (or vaccination) -shingles lesions are painful, often described as searing, burning, stabbing -pain may precede eruption by days to weeks -lesions resemble chickenpox but tend to become confluent -can have pain w/o rash -the rash has a unique unilateral dermatomal distribution aspect, does not cross center line, sensory field of infected neuron is involved with rash/ -"zoster" refers to belt or stripe -shingles not directly infectious but vesicles do contain VZV |
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What is the tx for shingles?
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-self-limited but painful
-VZIG does NOT prevent shingles -zostavax vaccination reduces pain and duration of shingles but it is a preventative therapy and NOT used to tx shingles outbreaks or post herpetic neuralgia -boosts VZV specific immunity and avoids shingles in pts -live, attenuated and has higher virus concentration that varivax (not for use in kids) -duration of efficacy unknown and the requirement for re-application remain to be established |
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What is the most common complication of shingles outbreaks?
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post herpetic neuralgia
-pain may persist for months and is more common in elderly |
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What are the cardinal signs of infection with HHV-6?
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sequence of high fever followed by eruption of a rose-colored rash
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Describe the HHV-6.
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-it is a beta-herpesvirus
-dsDNA -enveloped |
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How does HHV-6 replicate?
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-mostly in CD4 lymphocytes
-hypothesized to establish latent infections but site unknown (probably monocytes/lymphs) |
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Describe the clinical manifestations of HHV6.
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-one of the most regularly acquired viral infections of childhood
-sustained fever 2-5 days -defervescence is rapid and linked with the appearance of a maculopapular rash that involves the trunk and neck -complications rare |
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Describe HHV6 epidemiology.
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very high prevalence has been discovered by serological analysis
-virus is reactivated and shed in the saliva of adults that are immune suppressed, suggesting that reactivation/shedding is the source for childhood infections |
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What is "the fifth disease"?
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parvovirus B19
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Describe the clinical manifestations of the fifth disease (parvovirus B19).
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-prodromal illness of several days duration with mild sx including fever, HA, malaise, myalgia, resp. sx, N/V
-prodrome followed by a skin rash -characteristic slapped cheek appearance -rash exhibits circumoral sparing and resolves in 1-2 wks -rash may also involves limbs and trunk -CT manifestations are known, arthralgia/arthritis may follow, many adults may have arthritis or arthralgia alone w/o any other preceding sx |
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Describe parvovirus B19.
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-ssDNA
-no latent stage known -requires functions expressed only in host cell S phase and implies need for actively dividing cells -replication of this virus has never actually been demonstrated in any animal cells |
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Describe parvovirus B19 epidemiology.
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-only known human parvovirus capable of independently causing disease
-incubation period of 4-7 days -epidemics in late winter and spring -worldwide -exact mode of transmission not known but seems to persist well in environment -highest incidence in school age kids |
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How is diagnosis of parvovirus B19 made?
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-facial rash is helpful to confirm suspicion
-detection of anti B19 IgM ab using ELISA -PCR |
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What are fifth disease (parvovirus B19) complications?
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1)anemia-attacks erythroid progenitor cells
2)hydrops fetalis-virus infects and kills blood precursor cells |
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What is the tx and prevention for parvovirus B19 infection?
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-no vaccine
-most pts make a full and rapid recovery -Immunoglob. available for anemic pts -tranfusion therapy for aplastic crisis pts until immune response controls |
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Describe the orthopoxviruses.
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-large,brick shaped virions that are indistinguishable by EM
-DNA viruses that replicate in the cell cytoplasm in factories -virus is very independent of host functions -dsDNA -ex. include smallpox, vaccina, monkeypox, and cowpox |
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Describe smallpox (variola).
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-natural reservoir was humans
-virus was eradicated in 1977 -smallpox was developed as a biological warfare agent -most humans are now vulnerable to this even those that had the vaccine |
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Describe monkeypox.
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-clinically very similar to smallpox, africa only
-discovered as an outbreak of illness with rash in monkey colony in Denmark and recognized as human zoonosis in 1970 -squirrels are natural reservoir (tranmission to humans via monkeys in normal route) -person to person trans. limited - |
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Describe propionibacterium acnes.
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gram positive pleomorphic bacilli that forms short chains or clumps
-common aerotolerant anaerobe, normal skin flora esp. sebaceous glands -primary bacterium that causes acne -can also cause opportunistic infections in pts. with prosthetic devices and IV lines |
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Describe the general characteristics of S. aureus.
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gram positive, catalase positive cocci, beta-hemolytic, MSA
-part of normal flora of perineum, axilla, nares -localized infection causes abscesses |
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Describe the toxins of S. aureus.
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1)exfoliative-causes outer layer of skin to slough off
2)pyrogenic-TSST1 (toxic shock syndrome) |
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Describe the enzymes of S. aureus.
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1)coagulase-clots plasma and localizes infection
2)hemolysins-lyse blood cells 3)leukocidin-damages eukaryotic membranes-necrotic pulmonary disease 4)hyaluronidase-spreading factor (CT)-invasin 5)staphylokinase=fibrolysin dissolves fibrin clots in the host-invasin |
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Describe the general characteristics of S. pyogenes.
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gram positive cocci
-GABHS most frequent strep skin pathogen -mostly spreading infections, but localized can also occur |
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What toxins does S. pyogenes have?
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1)Spe (strep pyrogenic exotoxins A-C and F)
-erythrogenic superantigens -cause the rash in scarlet fever 2)M protein-fimbriae/pili associated, impede phagocytosis and contribute to invasiveness -these ags create sequelae -M abs cross react with host cells and cause acute rheumatic fever (type II HS) -also generate ag/ab complexes and lodge in glomeruli (PSGN-type III HS) |
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What enzymes does S. pyogenes have?
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1)DNase-reduces viscosity of lysed cell contents
2)hyaluronidase-a spreading factor 3)streptokinase-spreading factor |
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What does the rapid strep test detect?
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the A (NAG-rhamnose) carb. in cell wall
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What are the main causes for acne vulgaris?
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1)genetics
2)follicular epidermal hyperproliferation due to androgen hormones 3)excess sebum production 4)P. acnes-produces pro-inflamm. mediators and diffuses through follicular wall 5)inflammation-release of fatty acids and HS to P. acnes |
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Describe the progression of acne vulgaris disease.
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-starts as a noninflammatory process
-begins with microcomedo (white or blackheads (closed or open)) formation-follicle opening, partially obstructed follicle by sebum, keratinocytes, hair -then moves to inflammatory process when the comedo contents rupture into dermis and release free fatty acids and initiate inflammatory response -papules are the mildest form of lesions (small firm pink bump), this is intermediate noninflammatory and flammatory acne -then get pustules which are clearly inflamed, contain visible pus (zits), chemical irritation arises from sebum -nodules are large and very painful, most severe form, inflamed pus filled lesions lodged deep within the skin |
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What is the tx for abscess forming skin infections such as acne?
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-retinoids which can be topical or systemic
-abx directed against P. acnes, less resistance when combined with benzoyl peroxide |
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What is folliculitis?
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-inflammatory cells w/in wall and ostia of hair follicle creates a follicular based pustule
-can be superficial or deep -superficial has multiple small papules and pustules on red base pierced by a central hair -deep lesions are red with fluctuant nodules -can occur on any hair bearing site |
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What are the 2 primary pathogens which cause folliculitis?
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1)S. aureus
2)P. aeruginosa-pyocyanin and pyoverdin, gram neg. |
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What are the forms of folliculitis caused by S. aureus?
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1)Barber's itch-Impetigo of Bockhart
-bearded area on upper lilp near nose -red follicular based papules or pustules which rupture and leave yellow crust, this is common b/c of staph in nasal passages 2)sty (hordeolum)-hair follicle of eyelid -Meibomian gland (internal) |
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Describe the type of folliculitis caused by P. aeruginosa.
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Pseudomonal-wetsuit-or "hot tub" folliculitis
-appears 8-48 hrs after exposure to contaminated water (inadequate chlorine) -typical signs in areas occluded by swimwear -systemic component includes fever, HA, sore throat, malaise, GI distress |
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What causes a furuncle (boils) and what are they?
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S. aureus
-small abscess that exudes purulent material from a single opening -involves skin and subcutaneous tissues -in area with hair follicles such as neck, axillae, butt |
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What causes a carbuncle and what is it?
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S. aureus
-aggregate of connected furuncles -several pustular openings, found on neck, back, thighs |
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What is the tx for folliculitis, furuncles and carbuncles?
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1)folliculitis-for recurrent use antibacterial soaps and hand washing
-for refractory or deep can use topical/oral abx (systemic abx must cover MRSA) 2)for furuncles/carbuncles use warm compress initially, removal of pus by incision and drainage, antimicrobials -for recurrent furunculosis give mupirocin (bactroban)-a topical cream applied to nares, axillae, and peritoneum for 5 days w or w/o clindamycin -always tx for S. aureus to prevent hematogenous spread of infection |
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What is pyoderma?
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a bacterial skin inflammation marked by pus filled lesions
-spreading infection confined to the dermis and epidermis |
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What are the forms of pyoderma?
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bullous and nonbullous impetigo (impetigo contagiosa)
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What causes nonbullous impetigo?
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S. aureus is primary pathogen
GAS is secondary -single red macule which rapidly evolves into vesicle/pustule and then ruptures, leaves yellow crusted exudate over erosion -infectious and spreads rapidly |
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What conditions encourage nonbullous impetigo?
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hot, humid weather
participation contact sports poor personal hygiene work environment -it is spread by contact or autoinoculation |
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What causes bullous impetigo?
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S. aureus exclusively
-rare infection from exfoliative toxin producing strains -superficial intraepidermal lesions which begin as vesicles and then form thin white blisters (bullae) which then rupture and crust -blisters contain exfoliatin producing S. aureus (toxin does not disseminate so only localized exfoliation) |
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In what population is bullous impetigo most common?
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young kids <2 yrs old on face and legs
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What causes ecthyma and what is it?
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caused by GAS
-ulcerative pyoderma which extends into the dermis, forms ulcers, greenish yellow crust, violaceous margins -RARELY CONTAGIOUS -results from untreated impetigo, preexisting tissue damage, immunocompromised, and poor hygiene -usually in kids, older folk, and immunocomp. -complications include pigmented scars from damage to dermis -occurs on lower extremities (can occur on face and arms tho) |
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What is the tx for impetigo and ecthyma?
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1)personal hygiene
2)gentle debridement 3)topical abx-mupirocin 4)systemic abx-first line: ceph, semisynthetic penicillin or beta lactam/lactamase inhibitor combo -for MRSA give TMPSMX, clinda, fluroroquinolone |
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What are the pathogens of cellulitis?
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-in immunocompetent adults it is GAS and occasionally S. aureus
-MRSA is increasing in IV drugs users, HIV, prisons, athletes, military trainees, etc -acinetobacter baumannii-emerging multidrug resistant infection (aerobic) -others include pasteurella multocida, aeromonas hydrophilia and legionella |
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What is crepitant cellulitis and what causes it?
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caused by gas production by clostridia or anaerobes (C. perfringens)
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What are the sx of cellulitis?
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-HALLMARK is heat, redness, edema, and tenderness (HEET)
-orange peel appearance, skin becomes hot and swollen -marked inflammation -regional lymphadenopathy may occur -may or may not have sx of systemic toxicity |
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What are the 2 categories for diagnosis of cellulitis?
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1)small areas of involvement, diagnosis: minimal pain, no signs of systemic infection, no risk factors for more serious illness
-if begin treatment immediately with positive response (complete lab workup prolly NOT necessary) 2)extensive areas of involvement or spreading, diagnosis: lab workup required, what you think is cellulitis may be a more serious infection such as necrotizing fasciitis or myonecrosis -ID the pathogen if possible, only IDed in 1/3 of cases but is useful for IDing unusual pathogens |
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What does a lab workup for cellulitis include?
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-gram stains of cultures from abscesses if present
-culture from sample aspirate -CT and MRI-rule out fasciitis and osteomyelitis |
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What is the tx for cellulitis?
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AS a rule: avoid NSAIDs for sx relief, they mask indicators of worsening disease and inhibit PMN cytokine release
-give abx -surgical debridement and draining pus, elevation and immobilization of affected limb |
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What are the complications of cellulitis?
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-bacteremia, systemic infection
-clostridial cellulitis may develop into myonecrosis |
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Describe cellulitis caused by GAS (group A strep).
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-if postoperative infection develops w/in 24 hours
-rapid progression due to spreading factors -this pathogen is more likely than S. aureus if there is no obvious portal of entry, no obvious primary site of infection |
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What are the risk factors for GAS cellulitis?
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skin lesions (varicella)
immunocompromise immunodeficiency chronic steroid use |
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Describe S. aureus as a cellulitis causing pathogen.
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-frequent cellulitis pathogen
-does NOT spread as fast as other forms of cellulitis b/c has fewer spreading factors -associated with local abscesses -folliculitis can progress to cellulitis -lab results will show Gram +, beta hemolytic, cocci clusters, coagulase positive, catalase positive, rapid staph kit tests for coagulase and protein A |
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Describe Acinetobacter baumanii and its relation to cellulitis.
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-it is an uncommon cause of cellulitis
-aerobic broad gram neg. rods to coccobacilli -associated with trauma and use of invasive devices (gunshot wounds, central venous catheters) -has emerged from an organisms of questionable pathogenicity to an infectious agent of importance in hospitals worldwide (MDR pathogen) |
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Describe Pasteurella multocida and its relation to cellulitis.
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-an uncommon cause of cellulitis
-normal flora in the mouths of dogs and cats -suspect if cellulitis is associated with cat or dog bite -develops w/in 2-12 hrs of bite -associated purulent drainage -NOT CAT SCRATCH FEVER (bartonella henselae) |
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Describe how cellulitis can be caused by fresh and salt water bacteria that contaminate wounds.
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-fresh water organisms such as aeromonas hydrophilia and legionella
-saltwater organisms such as vibrio vulnificus |
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What is erysipelas and what pathogen causes it?
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a special form of cellulitis
-primarily caused by GAS -S. aureus is rare but recurrent infections |
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What are the sx of erysipelas?
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prodromal: malaise, chills, fever, systemic tox signs
-spreading, often painful red rash (bright red), apparent induration with sharp borders that do not blend, involvement of superficial lymphatics, lymphangitis -desquamation with resolution of erysipelas |
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Describe the epidemiology of erysipelas.
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-incidence is increasing due to new virulence factors
-seen in young, very old and immunocompromised -preexisting lymphedema is a risk factor -it is rarely fatal but fatality increases if associated bacteremia -most common on lower extremities, on face about 10% of ppl in butterfly distribution -in classic disease form, no workup necessary |
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What is the tx for erisypelas?
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begin abx (pen G for GAS but be aware of increasing drug resistance)
-keep affected limbs elevated, no immunity so recurrent infection possible |
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What part of the skin layer does the pathogen attack in necrotizing fasciitis?
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-directly attacks superficial and deep fascia, does NOT attack muscle
-not recognized as a contagious disease but group incidences have been observed |
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How is necrotizing fasciitis categorized and what are the categories?
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categorized by pathogen
type 1:polymicrobic type 2: monomicrobic |
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Describe type 1 necrotizing fasciitis.
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-polymicrobic, damage from synergistic activity of anaerobe/aerobe
-btwn 4-6 different organisms from a single abscess -most common facultative anaerobes: S aureus, E coli, pseudomonas, strep milleri, GAS, saltwater wound contamination by vibrio -most common anaerobes bacteroides, clostridium, peptostrepto, prevotella, and normal flora! (endogenous infection) |
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What are the type 1 necrotizing fasciitis risk factors?
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-exposure to recent surgery and trauma
-host factors such as diabetes mellitus -site of infection usually develops in trunk, abdomen, or perineum |
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What is Fournier's gangrene?
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a subtype of necrotizing fasciitis of the male or female genitalia
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Describe type II necrotizing fasciitis.
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-monomicrobic
-GABHS with M proteins 1/3 -hx of exposure usually not found -can follow blunt trauma, bug bite, chickenpox, IVDA, surgery -may occur as part of STSS or with NO initial signs of shock or organ failure |
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What are the type II necrotizing fasciitis risk factors?
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pt often immunocompetent and has NO significant PMH
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What are the clinical manifestations of necrotizing fasciitis?
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-initial pain is out of proportion to other clinical findings
-cutaneous anesthesia seen as nerves are damaged -hard wooden feel of subcu. tissues, fascial planes and mm groups not palpable -erythema-skin changes color over time (red to purple to blue) -fluid filled bullae may form -systemic toxicity, behavior appears as confused and in an altered mental state -detection of gas in tissues (crepitance with type 1), CT and MRI determine extent of infection -putrid odor ONLY with anaerobic pathogen |
|
|
How is diagnosis of necrotizing fasciitis made?
|
-failure to respond to abx therapy (need to differentiate from cellulitis which responds in 24-48 hrs)
-biopsy of tissue will determine extent of infection, gram stain to ID pathogen -tissue appearance during surgery, fascia swollen and necrotic (dull gray to yellow green color) -NO true pus anywhere -extensive undermining of surrounding tissue -separation of necrotic tissue along fascial planes |
|
|
What is the tx for necrotizing fasciitis?
|
-debridement, resect all necrotic tissue
-incise fascial planes until extent of damage is exposed including gas pockets -empiric abx tx for type I and II (different for each type) -hyperbaric Oxygen therapy (controversial) -maggot therapy used on some cases |
|
|
Describe the mortality of necrotizing fasciitis.
|
-death may occur w/in 24-96 hrs
-overall morbidity and mortality 70-80% -fournier gangrene mortality much higher |
|
|
What are the complications of necrotizing fasciitis?
|
-bacteremia, TSS, about 50% exhibit DIC, endotoxin shock (gram neg. infection), cutaneous gangrene and myonecrosis
|
|
|
What is type III necrotizing fasciitis?
|
myonecrosis=life threatening mm. infection
-develops contiguously from area of trauma, hematogenously from GI tract -most infections are caused by clostridium (gas gangrene), GAS (myositis) |
|
|
What is spontaneous gangrenous myositis?
|
a rare infection with rapid progression and high mortality
-enters through abrasions and blunt trauma -occurs equally in all age groups of HEALTHY ppl, men and women equal -no increased risks in ppl with diabetes and immune defic. -NSAIDS predispose and reduce signs and sx -vimentin, an upregulated surface molecule on injured mm increases the adherence of GAS (site of previous trauma like a strain) |
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|
What are the signs/sx of spontaneous gangrenous myositis?
|
fever, pain, tenderness, board like induration of the mm, skin is red, warm, petechiae, bullae and vesicles
-infection progresses and involves contiguous mm and subcutaneous tissues -rapid development into systemic tox with hypotension and signs of shock -NO gas formation in tissues |
|
|
How is spontaneous gangrenous myositis diagnosed?
|
-histopathology
-requires immediate surgery to inspect deep tissues -findings in surgical specimens of degen. and necrosis of sk. mm .fibers, infiltration of granulocytes, numerous gram-positive streptococci |
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|
How is spontaneous gangrenous myositis treated?
|
-carries a 80-100% mortality despite proper tx
-aggressive surgical debridement as soon as diagnosis is considered -possible limb amputation -abx: clindamycin better than pen G b/c it suppresses toxin synthesis and inhibits M protein synthesis (facilitates phagocytosis) -immunotherapy (efficacy unknown) |
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|
What is clostridual myonecrosis ?
|
AKA gas gangrene
-caused by several spp -endospore forming anaerobic bacilli -short doubling time (divide every 8-10 mins) -C. perfringens type A causes 90% of gangrene infections, found in soil and human feces -also a cause of cellulitis and fasciitis w/out myonecrosis |
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Describe the pathogenesis of clostridial myonecrosis.
|
-develops <3 days after injury b/c has very short doubling time
-entry of pathogen vegetative cells or spores occurs during the initial insult -there is traumatic and surgical gas gangrene via direct inoc. of wound -there is also spontaneous (non-traumatic) gas gangrene from hematogenous spread from GI tract, often associated with malignancy (C. septicum is the most frequent pathogen) -bacterial exotoxins and other factors cause the pathogenesis |
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|
List the bacterial exotoxins and factors responsible for the pathogenesis of clostridial myonecrosis.
|
1)alpha-toxin-similar homology to PLP C
-lecithinase-cytotoxic and destructive to membranes and primarily responsible for C. myonecrosis sx -lyses RBCs and other cells, decreases force of cardiac contraction, triggers histamine release, platelet aggregation, and thrombus formation (all C. perfringens produce this toxin but type A produces most.) 2)theta toxin-perfringolysin- 3)kappa toxin-a collagenase 4)gas production 5)oxygen depletion |
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Describe the function of theta toxin in C. perfringens.
|
perfringolysin
-causes direct vascular injury, cytolysis, hemolysis -leukocyte degeneration and PMN destruction -may explain poor host inflammatory response and absence of inflammatory cells in biopsies |
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|
Describe kappa toxin of C. perfringens.
|
-a collagenase
-facilitates rapid spread of necrosis through tissue planes -all species of Clostridia produce many other factors including degradative enzymes such as collagenases, DNases, hyaluronidases and proteases |
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What regions of the body are typically affected by clostridial myonecrosis?
|
90% of cases are on the extremities
-10% of cases on the trunk, primarily trauma and surgery |
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|
What are the systemic findings of clostridial myonecrosis?
|
bacteremia is RARE
-mediated by blood borne alpha toxin which promotes shock and vascular leakiness leads to release of PAF and TNF -DIC may result-clot formation then bleeding -Cardiac output drops, PMNs killed |
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|
What are the symptoms of clostridial myonecrosis?
|
-acute onset with fulminant course
-typical incubation <24 hrs -skin at affected site is pale-red-bronze with bullae which appear blackish green |
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|
How is diagnosis of clostridial myonecrosis made?
|
-sudden onset with severe worsening pain
-thin hemorrhagic exudate with sweet mousy smell (C. perfringens) -foul odor with mixed culture (nonclost. myonec) -low grade fever -toxemia with tachycardia -gas pockets in tissues are NOT diagnostic of clostridial gangrene b/c other organisms produce gas as well -crepitation -definitive diagnosis made by large gram variable bacilli at injury site, gram pos. in culture -microscopic eval. of biopsy will reveal degenerating mm. bundles, microbes, and characteristic ABSENCE of inflammatory cells -CT or MRI shows extent of gas pockets -C. perfringens has a double zone of hemolysis |
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|
How is clostridial myonecrosis treated?
|
-care of wounds along with surgical debridement
-delay primary suturing to allow O2 exposure -empiric abx cover GAS, clostridium spp, mixed anaerobes/aerobes -if definitive for C. perfringens give combo of penicillin and clindamycin -HBOT and amputation |
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|
What is the mortality of clostridial myonecrosis?
|
20-30% w/tx
100% w/o tx |
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|
Decribe nonclostridial myonecrosis.
|
-flora includes anaerobes like bacteroides and peptostreptococcus and aerobes like S. aureus
-the prognosis of this is much better |
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|
What is staphylococcal scalded skin syndrome?
|
a syndrome of toxin-mediated dermatitis with superficial blistering and exfoliation
-follows a red rash -caused by S. aureus |
|
|
What toxins are responsible for Staphylococcal scalded skin syndrome?
|
-exotoxins secreted by S. aureus
-2 different superantigens 1)epidermolytic toxins (ET-A on a chromosome and ET-B on plasmid), both are serine proteases |
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|
What is the action of the SSSS epidermolytic toxin?
|
-produces intraepidermal splitting of tissues and necrosis
-it cleaves desmoglein1 (important in desmosomes and mediates keratinocyte adhesion) -affects large portions of skin -same toxin as in bullous impetigo but SSSS the toxin is systemic and in bullous impetigo the toxin is localized -role of the toxin is unclear but may help spread of S. aureus |
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|
Describe the epidemiology of SSSS.
|
-epidermolytic positive strains are rare (5%)
-children <5 yrs common -more common in neonates (introduced by asx adult carrier) -very rare in adults -more likely in immunocompromised and adults with renal failure (that is how the toxin is cleared) |
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|
Describe the progression of SSSS in infants.
|
-the site/focus of infections is oral/nasal cavities, throat, umbilicus, conjunctiva
-early stage see fever, irritability, faint orange-red macular tender blanching rash -acute stage 24-48 hrs the rash progresses to a blistering eruption, mucus membranes become hyperemic, conjunctivitis may develop, tissue paper like wrinkling of epidermis, then large flacced bullae/blisters form -Nikolsky's sign (pressure applied to skin with finger causes separation of upper epidermis) -followed by sheet like desquamation, culture of lesions will show no S. aureus -decline stage (5-7days later), lesions heal with no scarring (adults are frequently followed by bacteremia and pneumonia) |
|
|
How is diagnosis of SSSS made?
|
-definitive diagnosis made by culture and biopsy results
-culture all pts. conjunctiva, feces, skin, etc -ID pathogen and determine abx sensitivity -examine frozen sections of lesions -ID toxins by latex agglut. or ELISA |
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|
How is SSSS treated?
|
-eradicate the focus of infection with abx
-DOC is initial IV, penicillinase resistant antistaph. abx -supportive care, give cream to improve barrier function of skin, maintain fluid and electrolyte balance |
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|
What precautions must be taken in neonatal units to prevent SSSS?
|
-strict hand washing, abx soap (chlorhexidine)
-barrier nursing protocols -search for asx carriers (40% carry in nasal; lower in hands, perineum, axilla) -mupirocin application (eradicate nasal carriage) |
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|
What are the main clinical characteristics of the toxic shock syndromes?
|
acute febrile illnesses
characterized by erythematous eruption accompanied by systemic involvement |
|
|
What is the source of staphylococcal toxic shock syndrome?
|
1)hyperabsorbent tampon induces TSST1
-increase pO2 of vagina, supply surfactant and bind Mg -not just menstrual associated tho 2)postpartum and surgical wound infections 3)packing of surgical wounds 4)sinusitis, arthritis, etc kids can have it on skin and in nonsurgical lesions >90% are menstrual related |
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|
What is the cause of TSS?
|
toxins produce the clinical manifestations
-TSST1 -other superantigens like staph enterotoxin B and A -pts with TSS lack abs to TSST1 and fail to develop abs in convalescent serum -gamma IFN inhibits polyclonal Ig production to TSST1 |
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|
What is the cause of sx in STSS?
|
strep pyrogenic exotoxin producing strains (SPEA primarily)
-streptolysin O-synergist with SPEA for TNFalpha and IL1 -M type protein -mucoid colonies with hyaluronic capsules |
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|
Describe the pathogenesis of STSS.
|
-linked to invasive diseases such as necrotizing fasciitis, cellulitis, myositis
-also have absence of protective immunity -predominately in young adults with a vigorous immune response -untreated young and very old more likely to succumb to TSS/STSS |
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|
What are the predispositions for STSS?
|
same as type II necrotizing fasciitis
-has a 50% co-occurrence with STSS -strep. myositis |
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|
How is the diagnosis of TSS made?
|
for S. aureus TSS there must be fever, rash, desquamation (1-2 wks after, usually palms/soles), shock/hypotension (orthostatic syncope), multisystem involvement (3 or more of GI, mm, mucous membrane hyperemia, renal, hepatic, blood, CNS)
-confirmed diagnosis meets lab criteria and has 5 of 5 clinical manifestations and desquamation |
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|
Describe the CDC case definition for diagnosis of STSS.
|
-S pyogenes causative agent
-hypotension -multi organ involvement (2 or more); renal, coagulopathy (platelets or DIC), hepatic, ARDS, rash, soft tissue necrosis -isolation of GAS - a confirmed case meets the clinical case definition and there is isolation of GAS from sterile site |
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|
What is the tx for TSS/STSS?
|
1)O2/respiration (optimize tissue oxygenation)
2)IV fluids-normalize flow and perfusion 3)IVIG-effective neutralization of TSS toxin 4)abx-S aureus TSS give empiric IV clindamycin and vancomycin -for S. pyogenes GAS STSS give empiric IV clindamycin and cabapenem or peniciliin plus beta-lactamase inhibitor -in IDed GAS give clindamycin and pen G |
|
|
What conditions do anaerobes prefer?
|
-they prefer acidic conditions and low O2 tension
-necrotic tissue is acidic due to lactic acid fermentation -predisposing medical conditions create habitats such as compromised circulation, diabetes, trauma |
|
|
What are the endogenous and exogenous sources of anaerobes?
|
endogenous: infections arise from contamination of endogenous bacteria into contiguous or other sites (orodental, aspriation pneumonia, intraabdominal infection)
exogenous sources: soil, food, water (ex. C. perfringens, C. tetani, botulinum) |
|
|
What is diagnostic of anaerobic infection?
|
putrid odor from infections and discharges but it is a late feature in developing infection
|
|
|
Describe the general characteristics of bacteroides.
|
most common non-sporeforming opportunistic anaerobic pathogen
-bile resistant -several different species exist |
|
|
Describe the characteristics of Bacteroides fragilis.
|
-slim,pale staining gram negative bacillus
-encapsulated -most common cause of bacteroides infections (genital, GI, and abdominal) -relatively hardy organism, easily cultured -LPS-no lipid A -less toxic than other gram negs. b/c of altered structure of lipid A |
|
|
What are the virulence factors of Bacteroides fragilis?
|
1)polysaccharide capsule-antiphagocytic, stim. abscess formation, inhibits macrophage migration
2)fimbriae-promote adherence to host cells 3)Beta-lactamases-chromosomal and plasmid antibiotic resistance genes -these are the EXCEPTION to the rule and have SOD and inducible catalase so they survive O2 tissues and ROS attack 4)succinic acid-inhibits PMNs 5)IgA protease (degrades IgA in mucous membranes) 6)extracellular enzymes which promote abscess formation (collagenase, fibrinolysin, heparinase, etc) |
|
|
Describe the epidemiology of bacteroides fragilis.
|
-infections are endogenous and caused by normal flora
-high # of clinically significant infections, polymicrobic infections with 1+ facultative anaerobes -person to person transfer unknown |
|
|
Describe the pathogenesis of bacteroides fragilis.
|
-noninvasive
-diplacement by trauma; disease state -wall of colon-localized abscess -rupture through to peritoneal cavity will cause peritonitis -its activity is promoted by other bacteria in abscess (such as enterobacteriaceae) -can also spread through the bloodstream onto other organs |
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|
Describe the clinical manifestations of bacteroides infection.
|
-deep pain and tenderness below the diaphragm, fever and findings of acute abdomen (sudden, severe ab pain <24 hr duration)
|
|
|
How is bacteroides infection tx?
|
drainage of abscess and debridement of necrotic tissue
-abx, susceptible to metronidazole, clindamycin but resistance increasing -give combo that inhibits cell wall synthesis |
|
|
Together, what make up the second most common anaerobic pathogens?
|
porphyromonas and prevotella
-both are encapsulated, produce LPS, and produce IgA, M, and G proteases |
|
|
Describe porphyromonas.
|
gram neg bacilli
-normal oral flora (also GI and GU) -fimbriae -cause gingival and periapical tooth infections |
|
|
Describe prevotella.
|
gram neg. pleomorphic bacilli
-has capsule -P. melaninogenica produces a black pigment and causes URT -P bivia and disiens in female genital tract -form polymicrobic infections with facultative AGNR (enterobacteriaceae), peptostreptococcus, fusobacterium |
|
|
Describe fusobacterium.
|
gram neg. bacilli
-fusiform (cigar shaped with pointed ends) -normal flora of oral cavity -biochemically different than other gram neg. anaerobes, produces odiferous H2S and methylmercapton |
|
|
What are the clinical manifestations of fusobacterium infection?
|
-polymicrobic soft tissue infections
-gingivitis (ANUG)-trench mouth -Noma which is a ravenous gangrene infection of the face (malnutrition associated) -monomicrobic infection causes osteomyelitis |
|
|
Describe peptostreptococcus.
|
-gram pos. coccus
-nonmotile chaining cocci -normal flora on mucocutaneous surfaces such as mouth, intestinal tract, vagina, urethra, and skin |
|
|
Describe the clinical manifestations of peptostreptococcus.
|
-opportunistic pathogen seen in aspiration pneumonias, brain abscesses, GI and wound infections
|
|
|
What are some clues for diagnosing anaerobic infections?
|
-infections contiguous to a mucosal surface
-foul or sickly sweet smelling discharge -severe tissue necrosis with fasciitis -abscess formation or gangrene -gas production-blebs/bullae or crepitant skin is ONLY A CLUE b/c other facultative anaerobes produce gas too -do a gram stain of exudate, will usually show mixed population (some with unique morphology like fusobacterium) -lack of abx responsiveness |
|
|
What are the generalized guidelines for location of anaerobic infections in the body?
|
-above the diaphragm: fusobacterium, prevotella, and peptostreptococcus
below the diaphragm: bacteroides |
|
|
What are the tx for anaerobic infections?
|
-drain abscesses surgically or percutaneously
-take samples carefully, prevent normal flora contamination -surgical or medicinal maggot debridement -leave abscess open to air so it will have O2 exposure -HBOT therapy -abx (anaerobic infections create acidic and low O2 environments) abx must penetrate tissue so IV delivery may be necessary -can not use aminoglycosides b/c they are not effective in an acidic environment, can't use sulfa drugs, or penicillin -can use clindamycin, metronidazol, combo drug therapy, |
|
|
Describe the morphology of ringworms and onychomycoses.
|
hyphae and arthroconidia grow in dead keratinized tissue and feed on keratin
|
|
|
Describe the laboratory culture of ringworm and onychomycoses.
|
-best culture results for onychomycosis is specimen taken under nails
-culture on Sabouraud agar or dermatophyte test medium -grow at room temp (mature in 1-4 wks) -compared to bacteria, dermatophytes are slow growers -dermatophyte test medium is based on phenol red which makes early detection possible -some microsporum spp fluoresce under Wood's light -10% KOH or lactophenol cotton blue is useful for observing arthoconidia and hyphae in tissue |
|
|
What is the infective and diagnostic stage of dermatophytes?
|
arthroconidium
|
|
|
What is trichophytin?
|
crude antigen of dermatophytes
-carb component initiates immediate response -peptide component initiates delayed response -pts with immediate type or w/o delayed type rxn are more susceptible to chronic infections |
|
|
What are the clinical signs of dermatophyte infection?
|
-growth in keratinized tissue (hair, nails, outer skin)
-lesions will have inflammation at the edges, red and scaling, central clearing possible with hair loss, itching! |
|
|
What is the most prevalent dermatophyte in humans?
|
T rubrum
T. mentagrophytes is second |
|
|
What does dermatophytid mean?
|
-id =reaction
-dermal rxn to fungal ags -HSN at distal site -lesions are devoid of organisms, most common in tinea pedis -sometimes a result of excessive tx |
|
|
What agents will kill the spores of dermatophytes?
|
benzalkonium chloride
chlorine bleach detergents |
|
|
What is the most common pediatric dermatophyte infection worldwide?
|
trichophyton and microsporum
|
|
|
What type of conidia does microsporum have?
|
macro and micro
|
|
|
What causes tinea versicolor and describe the agent.
|
malassezia furfur
-it is a lipophilic yeast with unbranched hyphae and spherical cells -depigmented maculae -found mostly in young adults -will see "sun spots", areas of hypo and hyperpigmentation b/c tyrosinase inhibitors interfere with melanin production but also induce enlargement of melanosomes -topical miconazole is the preferred tx |
|
|
What is tinea nigra?
|
caused by hortaea werneckii
-brown skin lesions -tropics and subtropics of several continents -disease of kids and young adults (mainly females) -palms are often affected -septate hyphae are visible in KOH prep |
|
|
Describe sporothrix schenckii.
|
a subcutaneous fungus
-thermally dimorphic -has conidia-cluster resemble daisies -chronic granulomas and necrosis -DOC is amphotericin B or itraconazole |
|
|
Describe the pathophysiology of sporothrix.
|
traumatic inoculation
-develops as abscesses, nodules, or ulcers -occurs along lymphatics -usually self-limiting -this is a worldwide disease found on thorns, decaying wood, etc -occupational disease of gardeners and nursery workers |
|
|
How is ID of Sporothrix made?
|
-specimens consist of pus in lesions
-yeast is seldom detected in biopsy -clusters of conidia on Sabouraud agar - |
|
|
Describe tick paralysis.
|
-occurs after tick has fed for days
-paralysis is linked to some component in the female tick's saliva (conduction block occurs) -fatalities due to resp. paralysis -confused with polio or Guillain-Barre syndrome (afebrile early on) |
|
|
What is Norwegian scabies?
|
crusted lesions teeming with mites
-appear on head, neck, buttock and perianal region -associated with HIV |
|
|
How is Sarcoptes scabei diagnosed and treated?
|
apply mineral oil directly to infected area, scrape lesion, and visualize microscopically
-proof of scabies: whole mite or parts, eggs and scybala (fecal pellets) in scabies burrows -tx:permethrin or ivermectin -note that itching can persist for weeks after tx |
|
|
What is pediculus humanus?
|
head and body lice
-causes bite irritation and is a vector for epidemic typhus -tx: 1% permethrin -egg to egg cycle takes 3 weeks |
|
|
What is the transmissible form of Trichinosis?
|
larva
-then enter the body, mature into adults which then give rise to more larva which are also the destructive form |
|
|
What is the transmissible and destructive form of visceral larva migrans, cutaneous larva migrans, and anisakiasis?
|
the larva
|
|
|
What are the 2 cycles through which trichinella can be transmitted?
|
1)domestic cycle with pig, rat, dog, etc
2)sylvatic cycle with bears, raccoons, etc -human cases are usually due to pork or bear meat consumption |
|
|
What are the 2 phases of trichinosis infection?
|
1)intestinal phase includes an inflammatory response to the adults, penetration of larvae, expulsion of adults
2)parenteral (tissue) phase includes an inflammatory response to the larvae and their entry into sk. mm. -the extent of the disease directly correlates with larval burden -there is eventual death and calcification of larvae in all sites but nurse cell formation permits longer survival in mm. -mm pain and dysfunction are classic features of disease |
|
|
How is diagnosis of trichinosis made?
|
-pt dietary hx important
-suspicion heightened due to presence of eosinophilia, periorbital edema, myositis, fever, diarrhea -do a mm. biopsy-provides definitive proof -serologic tests are useful to aid diagnosis |
|
|
How is trichinosis prevented?
|
-smoking, drying, or salting of meat will NOT kill larvae
-larvae are destroyed by adequate freezing, proper cooking |
|
|
What is the usual etiologic agent of visceral larva migrans?
|
toxocara canis, the common intestinal roundworm of dogs
-in utero infection occurs in the developing pup and adults worms develop in the infant pup |
|
|
What is the infectious form of the agent which causes visceral larva migrans?
|
ingestion of the eggs of toxocara canis
|
|
|
Describe the epidemiology of visceral larva migrans.
|
-primarily a pediatric problem
-eggs are very common in the environment |
|
|
What are the clinical characteristics of VLM?
|
-there is presence of fever, hepatomegaly, and lower respiratory sx
-evidence of pulmonary infiltration -presence of marked eosinophilia -usually a benign illness -ocular involvement can occur but more commonly seen in older kids and adults, larval death stimulates granuloma formation and can have a clinical resemblance to retinoblastoma |
|
|
How is the diagnosis of VLM made?
|
-hx of dog companionship is useful
-nonspecific lab findings include eosinophilia, hyperglobulinemia with presence of isohemagglutinins and Forssman ab -ELISA test using larval ags in reliable -definitive diagnosis depends on positive biopsy result |
|
|
Describe the etiology of cutaneous larva migrans.
|
usual agent is ancylostoma caninum, the canine hookworm
-infection in humans results from larval penetration of skin |
|
|
Describe the epidemiology of CLM.
|
-in US, most cases are reported from teh southeastern branch areas but canine hookworms are common nationwide
|
|
|
What are the clinical manifestations of CLM?
|
-there is appearance of a linear burrow, linear papules, or papulovesicular lesions
-lesions are elevated, red, and serpiginous -itching is intense (danger of secondary bacterial infection) -most cases are self-limited |
|
|
How is diagnosis of CLM made?
|
usually based on clinical appearance
-lesions may be atypical and must be differentiated from those due to other agents such as fly larvae |
|
|
Describe the cause of anisakiasis.
|
-disease is due to the larvae of various nematodes of marine mammals
-larvae are found in the tissues of squid and various marine fishes -more serious disease is due to anisakis spp. |
|
|
Describe the epidemiology of anisakiasis.
|
-occurrence of disease requires ingestion of raw or improperly prepared fish or squid dishes
-most reported cases occur in Japan -sporadic reports worldwide |
|
|
What are the clinical manifestations of anisakiasis?
|
-larval penetration of the mucosa and submucosa is followed by worm death and eosinophilic granuloma formation
-clinical pres. is variable depending on duration of infection, location in GI tract, spp of worm, etc -acute disease is asx or may present with epigastric pain, N/V, sx can mimic appendicitis or peptic ulcers |
|
|
How is diagnosis of anisakiasis made?
|
-sudden signs of gastritis commonly seen
-radiographic evidence of a gastric or intestinal mass -eosinophilia is uncharacteristic but leukocytosis is common! -gastroscopy and excision of the mass will reveal a larva at the center of the lesion following microscopy -serology and skin tests have been useful in chronic cases |
|
|
What is Baylisascaris procyonis?
|
a common intestinal roundworm of raccoons
-groups of raccoons defecate in common areas called latrines -there is contamination of the environment with feces and eggs and the eggs are then ingested by humans -the juveniles are rather aggressive and wander prior to their death, have a strong tendency to enter CNS and eyes -permanent neurologic sequelae, blindness and death can occur |
|
|
How is Baylisascaris diagnosed?
|
-usually based upon epidemiologic information and exclusion of other causes
-no specific diagnostic test readily available |
|
|
What causes Baylisascaris infection?
|
a common nematode of raccoon causing a form of VLM
-CNS involvement esp. noted in kids |
|
|
What diseases does the Ixodes tick transmit?
|
LYme disease and babesiosis
|
|
|
What diseases does the Dermacentor tick transmit?
|
CTF, RMSF, tularemia
|
|
|
What diseases does the Amblyomma tick transmit?
|
tularemia, lyme, RMSF
|
