immuno 3

Infectious disease

a disease by which a microoragnism gains entry into the host, replicates inside the host, until the host is contagious enough to spread the disease and start the cycle over again

Histoplasmosis fungal infection

caused by Histoplasma capsulatam, found in soil contaminated with chicken,bird and bate feces

Aspergillosis Fungal infection

caused by Asperigillus species, usually secondary to other diseases can cause allergic reaction and infections can be invasive

Coccidioidomycosis fungal infection

caused by Coccidiodes immitis, also known as valley fever, desert fever or San Joaquin fever,

North America Blastomycosis fungal infection

caused by Blastomyces dermatitidis, an infection usually secondary to another disease, infection causes tumors in the skin or lesions in the lungs, bones, subcutaneous tissues, liver, spleen and kidney

Sporotrichosis: fungal infection

caused by Sporothrix schenckii, a disease manifest in three forms: lympathic, disseminated and repiraratory, infection is characterized by a sporotrichotic chancre

Dengue fever

vector borne diseased transmitted by the Ades aegyti mosquito, high fever, rash, muscle and joint pain, in severe cases there is serious bleeding and shock, liver: AST and ALT are extremely elevated, CNS: impaired consciousness, detection: Dengue virus nuclei acid (DENV) in serum, plasma, blood, CSF and other body fluid or tissue: IgM and IgG: anti-DENV

what does TORCH stand for

Toxoplasmosis, other viruses (HIV, Hepatitis), Rubella, Cytomegalovirus, Herpesvirus, Syphilis

Toxoplasmosis

the causative agent is toxoplasma gondii recognized as a tissue coccidlan (intracellular parasite), definitive host being the cat, it is usually transmitted to humans when the oocystys from cat feces are accidently ingested

Toxoplasmosis pathogenicity and transmission

Antibodies are not protective from parasites, latent activation may occur when immune suppression or compromise occur, T gondii causes damage to the heart, brain, eyes, as well as the central nervous system, raw milk

Toxoplasmosis is a

protozoan parasitic infection

all mammals can transmit T gondii

transplacentally

Toxoplasmosis congenital infection

1st trimester: CNS is delvoping usually ends in fetal death, 2nd trimester: hydrocephaly, blindness and other neurological damage, newborn: may be asymptomatic, can result in CNS malformation high igM levels are diagnostic, adults and children: mostly asymptomatic resembles infectious mononucleosis, because of the increased number of variant lymphocytes

Serological testing for Toxoplasmosis

Test of choice is the IgG testing, appears 1-2 weeks after initial infection, IgG peaks about 6-8 weeks, IgG declines gradually over the next 1-2 years

Treatment and prevention toxoplasmosis

pyrimethainine (Daraprim), sulfadiazine (antibiotic), prevention should be a concern for pregnant women and immunocompromised

IgM antibodies to T gondii in an adult are indicative of

current and recent infection

Rubella

Rubella is also known as German measles or 3 day measles, it is caused by an enveloped, single stranded RNA virus of the Togaviridae family, because of the virus is endemic to humans the disease is highly contagious, transmission: inhalation of respiratory secretion the incubation period of acquired rubella infection is 10-21 days and 12-14 is typical, infected persons are usually contagious for 12-15 days, which include the 5-7 days before the characteristic rash appears

Rubella serological testing: IgG and IgM are associated with signs and symptoms

IgM: peaks at 7-10 days, dimishes over 4-5 weeks, presence in a single specimen indicated recent infection. IgG production occurs as signs and symptoms appear and increase rapidly in the 7-21 days, to check adult immune statis IgG is reported positive (immune) or negative (non-immune), if both IgM and IgG are negative then the patient has never had rubella or been vaccinated, possess the ability to agglutinate RBCs antibodies to rubella will prevent attachment of the virus to the RBC

Rubeola

Rubeola infection is known as measles, single-stranded RNA virus of the family paramyxoulridae

Rubeloa prevention

vaccine is in the form of a live, attenuated virus

Rubella infection is transmitted by

respiratory secretions

The risk of fetal amolalies in material rubella is highest at the

first trimister

Herpes family virus includes

Herpes simplex virus (HSV), Varicella Zoster (VZV), Cytomegalovirus (CMV), Epstein-Barr virus (EBV)

CMV is the

most common virus transmitted to fetuses

CMV transmission

direct contact with oral, respiratory, or intrauterine secretions, blood transfusion: there are three forms of transfusion acquired CMV: primary infection, reactivating infection, reinfection with a different strain

Primary infection of CMV

seropositive recipient is transfused with blood from a CMV antibody-positive or antibody negative donor

reactivation infection of CMV

Seronegative recipient is transfused with blood from actively or latently infected donor

Reinfection of CMV

CMV strain in the donor’s blood differs from the strain originally infecting the recipient

CMV infects which cells

Lymphocytes

Varicella-Zoster virus

The primary form presents as chickenpox, after the latent phase reactivating occurs as shingles

Streptococcus infections

Streptococci that contain cell wall antigens of Lancefield group A are known as S. pyogenes; members of this group are almost always beta-hemolytic

S. pyogenes pathogenesis Upper respiratory infection: Pharyngitis

Pharyngitis: sore throat, swollen tonsils, and fever which progresses rapidly; can produce pharyngeal erythema with purulent tonsillar exudate

S. pyogenes upper respiratory infection: Scarlet fever

the signs and symptoms of scarlet fever are those of pharyngitis, with the addition of a rash. Usually develops on second day of illness and subsequently

S. pyogenes upper respiratory infection: Impetigo

skin infection that begins as a papule. The lesions may itch and will eventually crust over and heal

S. pyogenes upper respiratory infection: Cellulitis

subcultaneous infection with group A streptococci associated with a warm, red, tender area that may be mildly swollen. Can worsen and cause severe complications

S. pyogenes upper respiratory infection: toxic shock syndrome

S pyogenes also the most common cause of necrotizing fascitis, or “flesh-eating” bacteria, associated with toxic shock syndrome which destroys the host’s connective tissue

S. pyogenes pathogenesis Poststreptococcal infections: Rheumatic fever

approximately three weeks after infection, one may suddenly experience fever, joint pain, migratory arthritis, and even heart damage; damage occurs when antibodies to streptococcal M protein cross-react with skeletal and heart muscle

S. pyogenes pathogenesis Poststreptococcal infections: Glomerulonephritis

Inflammation of the glomerulus of the kidney that may occur 10 days after a throat or skin infection because of cross reaction antibodies, immune complexes lodged in the glomeruli, exotoxins such as streptokinase, damage glomeruli

The hyaluronic capsule of S pyogenes has an M protein that is a major virulence factor

M protein inhibits phagocytosis

Morphologic characterestics of S pyogenes: Streptolysin O

oxygen-labile enzyme

Morphologic characteristics of S pyogenes: Streptolysin S

oxygen-stable enzyme

Serologic assays for extracellular enzymes or toxins: in addition to throat and nasal cultures, antibodies to bacterial toxins and other extracellular products can be tested to detect the presence of a strep infection

Anti-streptolysin O (ASO), Anti-DNase B, streptozyme test, an elevated titer indicates a relatively recent infection, a declining titer represents a trend toward recovery, a constant low titer indicates a past infection

Anti-DNase B

Antibodies to DNase B is the most reliable immunologic test for recent S pyogenes skin infection

substances produced by S pyogenes include all the following

hyaluronidase, DNase A, B, C, D, erythrogenic toxin

An elevated antistreptolysin O (ASO) titer indicates

recent streptococcal infection

Laboratory diagnosis of S pyogenes can be made by

culturing of throat or nasal specimens, ASO procedure, Anti-DNase B

Serologic testing for S pyogenes should compare acute and convalescent specimens collected

2 weeks apart

Streptococcus agalactiae (group B streptococcus)

S agalactiae is the leading cause of neonatal sepsis in the United States, most commonly isolated from blood, screen is usually performed on pregnant women ages 35-37 weeks of gestation

Syphilis overview

a venereal disease caused by the spirochete Treponema pallidum

Syphilis transmission

Direct contact between humans through abraded skin or mucus, usually through sexual contact, incubation period is about three weeks

Congenital syphilis

cord blood may be used for screening, but must be repeated with heelstick specimen if positive

primary syphilis

a visible painless lesion, called a chancre occurs at the site of contact

Secondary syphilis

occurs if left untreated can form within 2-8 weeks, but occasionally as long as 6 months, high levels of antibody are produced at this time usually resolves within 2-6 weeks, even in the absence of therapy

Latent syphilis

usually beings after the second year of untreated infections and is characterized by a lack of clinical symptoms

Tertiary or late syphilis

occurs years after secondary syphilis it has three major manifestations: Gummas localized granulomas or lesions affecting the skeletal, cardiovascular disease with destruction of the elastic tissue in the aorta, Neurosyphilis, CSF is examined for diagnosis of tertiary syphilis

teritary syphilis is best evaluated by using

cerebrospinal fluid

detection of syphilis

direct testing of the organism, darkfield microscopy, direct fluorescent antibody (DFA)

non-treponemal methods of diagnosing syphilis

reagin: non-treponemal antibody like substance produced by syphilis infected patients against components of their own or other mammalian cells, non-treponemal antibodies are also called reagin antibodies

Flocculation test: rapid reagin (RPR) principle

Reagin reacts with cardiolipin, a lipid-rich extract from beef heart, as well as other animal lipids, read macroscopically

Flocculation test: Venereal disease research laboratories (VDRL)

CSF only is tested by this method, a reactive result is diagnostic of neurosyphilis

Treponemal methods for Syphilis serology

Chemiluminescent immunoassays/enzyme immunoassay (CIAs/EIAs), Treponema pallidum antibody IgG by ELISA, Fluorescent treponemal antibody absorption (FTA-ABS)

Treponemal methods of Syphilis (confirmatory)

Indirect immunofluorescence assay (IFA), Treponema pallidum particle agglutination (TP-PA), Treponema pallidum antibody IgG by immunoblot (western blot), PCR

direct examination of treponemes is most often performed with

darkfield microscopy

The substance detected by the RPR assay is

reagin

A term for nontreponemal antibodies produced by syphilis infected patients against components of their own or other mammalian cells is

reagin antibodies

Ticks inject substances into the bite area:

anti-inflammatory substances, bacteria, spirochete, protozoa and viruses, toxins

lyme disease

is an infectious multi-systematic disease caused by infection with the spirochete, borrelia burgdorferi

Lyme disease transmission

to humans by the bite of one of several ixodes species ticks, the preferred host of the larval and nymph stages of the loxdes tick is the white footed-mouse, the white-tailed deer is critical for adult tick mating, but does not play a role in the life cycle of the spirochete

Immunologic manifestations of lyme disease

an increase in spontaenous suppressor cell activity and reduction in natural killer activity, monoculear cell antigen-specific repsonses develop during spirochetal dissemination, antibodies form include cyoglobulins immune complexes, antibodies specific to burgdorferi and anticariolipin, in the later course of lyme disease a subset of patient develop outer surface protein A, which has been linked to chronic lyme arthritis in patients who are HLA-DR4 positive

Lyme disease assays

Positive EIA’s must be confirmed by western blot

Western blot analysis

Western blot is used to verify antibody reactivity to major surface or flagella proteins of B burgdorferi

other testing for Syphilis

Later in the infection PCR is the best method for detection since it amplifies small amounts of DNA

What is the causative agent of Lyme disease

Borrelia burgdorferi

most cases of Lyme disease in the United States remain concentrated in the

northeastern region

Ehrlichiosis

Ehrlichiosis is a general term for human granulocyte ehrilichiosis (HGE) (now called anaplasmosis) and human monocytic ehrilichiosis, Ehrlichia ewingii and an Ehrichia phagocytophilia-like agent anaplasmosis, Ehrlichia chaffeensis is the etiologic agent of human monocytic ehrlichiosis (HME)

Signs and symptoms (1-2 weeks after tick bite) for human ehrlichiosis

fever, headache, chills, skin rashes, myalgias nausea, vomiting and anorexia are also common

diagnosis of human ehlichiosis

must be initially based on signs and symptoms, diagnosis tests based on the detection of antibodies will frequently appear negative in the first 7-10 days of illness, dx involves hematologic, hepatic and CNS evaluations chemistry panel: elevated liver enzyme levels, clinical history: recent tick bites

Diagnosis of human ehlichiosis definitive

definitive diagnosis is based on inclusions in luekocytes, morulae (microcolonies of ehrichiae) is found in WBC cytoplasm in 20% of patients

Human Ehrlichious serology

anaplasmosis: diagnosis is confirmed by either: seroconversion a fourfold rise in titer of paired acute and convalescent sera, single serologic titer higher than 1:80 in patients with a supporting history and clincal symptoms, detection of IgM alone should not be interpreted as recent exposure. HME: a serologic titer higher than 1:128 in patients with a supporting history and clincal symptoms, serum or CSF can be analyzed for IgM and IgG antibodies to Ehrlichia spp

lab detection of Human Ehrlichiosis

PCR detection of the E phagocytophila like agent of anaplasmosis represents the most sensitive and direct approach to diagnosis, PCR detection of E chaffensis includes the amplification of sequences with 16s ribosomal DNA

The disease that can be identified by wright’s giemsa stained slides showing modular inclusions within granulocytes is

ehrllichiosis

Rocky mountain spotted fever

tick-borne disease caused by the bacterium Rickettisia rickettsii, more than half of cases come from only five states: North Carolina, South Carolina, Tennessee, Oklahoma, Arkansas

Rocky Mountain spotted fever pathology

Virus enters the skin spreads to the blood and multiples in the endothelial cells or the vein and arteries, the first symptoms are fever and headache, rash (90% of the cases), other symptoms include nausea and vomiting

Rocky mountain spotted fever diagnosis

blood is not always useful for detection by PCR or culture, PCR or immunhistochemical staining can be performed on skin biospy taken from rash site, detectable antibodies are observed within 7-10 days of illness onset, gold standard serological test for diagnosis is IFA with R rickettsii antigen

Rocky mountain spotted fever IFA

First IgG IFA titer is typically low or negative, second titer is typically shows a four-fold increase in IgG antibody levels, Physicans requesting IgM serological titers should also request a concurrent IgG titer

Treatment and prevention for HME and RMSF

Doxycycline

Babesiosis overview

caused by microscopic parasites that infects RBCs known as Babesia species, most commonly Babesia microti, transmission is most common in the northeast and upper midwest and peaks during warmer months

Babesia signs and symptoms

incubation period is 7-21 days with clinical presentation variables, sometimes fetal depending on the species, fever, fatigue, hemolytic anemia

Babesia diagnosis

parasites resemble Plasmodium species which causes malaria, distinguished from plasmodium formation of tetrads of merozoites (maltese cross), a titer higher than 1:256 is considered diagnostic of acute infection

Babesia can be found in

peripheral blood

the feature that distinguishes Babesia from Plasmodium (malaria) seen in peripheral blood smears is

“Maltese cross”

Chikungunya disease

Chikungunya virus is transmitted to human through mosquito bites, spread by Ades aegypti and Ades albopictus

Chikungunya disease signs and symptoms, diagnosis

occurs 3-7 days after bite, fever and joint pain, other symptoms include headache, muscle pain, joint swelling, and rash, Chikungunya IgM and IgG antibody testing can be performed by reference lab using ELISA on acute and convalescent specimens, IgM suggest a new and active infection and IgG suggest a current or past infection

Dengue shock syndrome

Dengue hemorrhagic fever (DHF) and dengue shock syndrome are caused by any one of the four related viruses, transmittedby Aedes aegypti and Aedes albopictus mosquitos

Dengue fever signs and symptoms

high fever, rash, muscle and joint pain, in severe cases there is serious bleeding and shock which can be life threatening, liver: AST and ALT are extremely elevated, CNS: impaired consciousness

Diagnosis of Dengue Fever

detection of Dengue virus neclei acid (DENV) serum, plasma, blood, CSF, and other fluid or tissue, IgM anti-DENV, IgGG anti DENV

West Nile Virus

member of Japanese enchphalitis virus group of flaviviruses that causes febrile illness and encephalites, igM is evident in most infected patients 7-8 days after onset of symptoms and may persist for more than 500 days it is detectable by ELSA, IgM is evident 3-4 weeks after infection

Zika virus signs and symptoms

microcephaly leading to incomplete brain development and other severe fetal brain, eye defects, hearing deficts, imapired growth, Gulbilin-Barre syndrome, uncommon sickness of the nervous system

Zika virus diangosis

Trioplex real-time PCR assay, Zika MAC-ELISA to identify IgM-antibody

Aedes aegypti is the vector for

Zika, Chikgunyuna, Dengue fever