Glossary of Microbiology Exam 3 2

Start Studying! Add Cards ↓

acne- causative agent
Propionibacterium acnes under the right conditions.
P. acnes is normal flora on the skin, so it is not a transmissible infection. Groups that have a combination of factors that can result in acne, rather than the distribution of P. acnes.
1) Topical agents that enhance the sloughing of skin cells 2) Topical or oral antibiotics (erythromycin or tetracycline)—not so good because it’s another way to build up microbial resistance, low levels for a long time! 3) Oral contraceptive pills—debate on using estrogen on pre-menopausal and menopausal women to counteract the effects of menopause. But estrogen has its own effects—dangers of estrogen use! 4) Isotretinoin (Accutane)—only used as last resort, has severe side effects 1) Psychological depression. It will decrease sebaceous gland activity. It will decrease P. acnes growth.
a localized (more serious) staphylococci infection of subcutaneous skin.
abscess--causative agent
Staph aureus
results in the inflammation of a single hair follicle or sebaceous land progresses into a large, red, extremely tender abscess or pustule. Often occur in clusters on parts of the body such as the buttocks, axillae, and back to the neck, where the skin rubs against other skin or clothing. Also called boils
larger deep lesion sometimes as big as a baseball created by aggregation and interconnection of cluster of furuncles. It s usually found on the back of the neck, extremely painful and can even be fatal in elderly patients where they give rise to systemic disease.
a superficial infection of the skin that causes it to flake or peel off. Not a serious disease, but highly contagious, children are primary victims.
Impetigo--causative agents
Staphylococcus aureus (gram positive cocci in pair and clusters) and/or Streptococcus pyogenes, also known as Beta hemolytic Strep Lancefield A (gram positive cocci in pairs and chains). Both are Beta hemolytic
Impetigo--strep complications
streptococcal pharyngitis, scarlet fever, pneumonia, puerperal fever, necrotizing fasciitis, serious bloodstream infections, and poststreptococcal conditions such as rheumatic fever.
Impetigo-signs and symptoms
“Lesions” may look like peeling skin, crusty and flaky scabs or honey colored crusts most often found around the mouth, face, and extremities. Superficial and itchy.
Staphylococcus aureus: virulence factors for impetigo are exotoxins—exfoliative toxin A and B (break down cell to cell binding), enzymes coagulase (cause fibrin to be deposited around bacteria), hyaluronidase (breaks down connective tissue), staphylokinase (breaks down blood clots), DNase (digests DNA), lipases (breaks down lipids, helps to colonize oily skin), and most hospital strains have penicillinase. Streptococcus pyogens (beta hemolytic strep group A or Beta S group A): virulence factors are streptokinase, plasminogen-binding ability, hyaluronidase and M protein.
drugs that will kill either organism: topical mupriocin or oral cephalexin for widespread involvement.
a fast spreading infection of the dermis and subcutaneous tissue
Cellulitis--causative agent
Usually Staphylococcus aureus or Streptococcus pyogenes in healthy people, any bacteria and some fungi in immunocompromised patients.
Cellulitis--signs and symptoms
pain, tenderness, swelling, and warmth. Fever and swelling of lymph nodes may occur. Red lines leading away from area are visible.
Cellulitis treatment
mild cases respond well to oral antibiotics that target both Staphylococcus aureus and Streptococcus pyogenes. More involved infections and infections in immunocompromised patients need aggressive treatment with oral or IV antibiotics (cephalexin) or surgical debridement.
Erysipelas--causative agent
Streptococcus pyogenes
Erysipelas--signs and symptoms
Edema and redness of skin near portal of entry fever and chills. Lesion spreads outward; cutaneous lesions can remain superficial or produce long-term systemic complications.
Necrotizing fascitis
flesh eating disease...very invasive
Necrotizing Fascitis--signs and symptoms
Early stage—same as impetigo—spreads rapidly destroying tissue
Necrotizing Fascitis--pathogenesis
Staphylococcus aureus: virulence factors for impetigo are exotoxins—exfoliative toxin A and B (breaks down cell to cell bonding) enzymes coagulase (causes fibrin to be deposited around bacteria), hyaluronidase (breaks down connective tissue), staphylokinase (breaks down blood clots), DNase (digests DNA), lipases (breaks down lipids, helps to colonize oily skin), and most hospital strains have penicllinase. Streptococcus pyogenes (Beta hemolytic strep group A or BetaS grp A): virulence factors are streptokinase, plasminogen-binding ability, and hyaluronidase and M protein.
Necrotizing Fascitis--transmission
starts with a small wound or incision—bacterial strains causing this have special toxins and enzymes that give them greater invasiveness. They destroy connective tissue in the skin, allowing the bacteria to spread deeper into tissues. Can be polymicrobial.
Necrotizing Fascitis--treatment
IV broad spectrum antibiotics, debridement of wound. If the infection is in a limb and cannot be contained or controlled, amputation of the lim may be considered. Sometimes pooled immunoglobulins (antibodies) are given.
Staphylococcal Scalded skin syndrome
A dermolytic condition caused by S. aureus. Can be thought as a systemic form of impetigo—toxins enter the bloodstream and then travel to the skin.
SSSS causative agent
Staph aureus
SSSS signs and symptoms
Fever may precede skin lesions, starts as a focal infection in throat, eye, impetigo and toxins enter the blood stream and travel systemically to the skin. Starts as bullous lesions, eventually the top layers of epidermis peel off completely.
SSSS pathogensis
Exfoliative toxins A and B
SSSS treatment
immedate systemic antibiotics (cloxacillin or cephalexin)
is a chronic, progressive disease of the skin and nerves
Leprosy--causative agent
Mycobacterium leprae is a slender acid-fast bacilli. It is a strict parasite and the slowest of growing of the Mycobacterium species. It multiplies within host cells in large packets called globi at an optimum temperature of 30°.
Leprosy--chronic progressive disease of skin and nerves
It has chronic and severe complications due to the widespread dissemination of bacteria. It grows primarily in macrophages in cooler regions of the body (nose, ears, eyebrows, chin, and testes). It causes lepromas (granulomous thickenings) and loss of sensitivity that predisposes the patient to unrecognized injury, secondary infections, blindness and kidney or respiratory failure.
Chickenpox and Shingles
With chickenpox, skin lesions progress quickly from macules and papules to itchy vesicles, filled with a clear fluid. Shingles is the reemergence of the virus that was latent in the ganglia.
Chickenpox and Shingles---causative agent
Human Herpes virus 3 (HHV-3) also called varicella or varicella-zoster virus. It is an enveloped DNA virus
Chickenpox and Shingles--signs and symptoms
Chickenpox: after 10 to 20 days incubation—fever and rash appear the skin lesions progress from macules to papule to itchy vesicles filled with clear fluid. No fever prodorome; lesions are superficial; in centripetal distribution (more in center of body). Shingles—developed abruptly after reactivation. It is thought that the virus migrates down the ganglion to the skin; multiplication resumes and produces persistent vesicles. Inflammation causes pain and tenderness that can last for several months. Involvement of cranial nerves can lead to eye inflammation and ocular and facial paralysis.
Chickenpox and Shingles--prevention
Live attenuated vaccine available since 1995 and is recommended a single dose between the ages of 12 and 18.
Chickenpox and Shingles treatment
Uncomplicated cases are self-limiting. Secondary bacterial infections are treated with topical or systemic antibiotics. Oral acyclovir is administered to people considered to be at risk for serious complications within 24 hours of onset of rash.
has been eradicated from the world. This infection manifested itself as a rash in the pharynx, spreads to the face, and progresses to the extremities. Variola major is a highly virulent form of smallpox that causes toxemia, shock and intravascular coagulation. Variola minor is a milder form of the disease. The causative agent of smallpox is an orthopoxvirus, an enveloped DNA virus.
Smallpox causative agent
Variola virus, an orthopoxvirus, an enveloped DNA virus.
Smallpox prevention
A vaccine is available, but has a high rate of side effects. One person per every million people vaccinated will die as a result. One thousand have non-life-threatening, but serious reactions at the vaccination site or generalized illness.
Small pox treatment
no treatment: antiviral treatment is not effective.
results in oral lesions called Koplik’s spots and characteristic maculopapular exanthemum that erupts on the head and then progresses to the trunk and extremities, until most of the body is covered. The most serious complication is subacute sclerosing panencephalitis (SSPE), a progressive neurological degeneration of the cerebral cortex, white matter and brain stem.
Measles causative agent
a member of the Morbillivirus genes. It is a single-stranded enveloped RNA virus in the Paramyxovirus family
Measles prevention
MMR vaccine (measles, mumps, and rubella) contains live attenuated measles virus and confers protection for ~20years. Vaccine is recommended for children between the ages of 12 and 15 months, with a booster before the child enters school.
Measles Complication
Children develop laryngitis, bronchopneumonia, and bacterial secondary infections such as ear and sinus infections. Children afflicted with leukemia or thymic deficiency are especially predisposed to pneumonia because of their lack of natural T-cell defense. In a small percentage of cases, the virus can cause pneumonia. Affected patient are very ill and often have a characteristic dusky skin color from lack of oxygen. Occasionally measles progresses to encephalitis, resulting in various CNS changes from disorientation to coma. Permanent brain damage or epilepsy can result. A large number of measles patients experience secondary bacterial infections with Haemophilus influenzae, Streptococcus pneumoniae, or other streptococci or staphylococci. These can lead to pneumonia or upper respiratory tract complications.
Also known as German measles or 3-day measles can appear in two forms: postnatal and congenital (prenatal) infection of the fetus
Rubella causative agent
Rubivirus in the family Togavirus. A non-segmented single-stranded RNA virus with a loose lipid envelop with different viral proteins. Humans are the only natural host.
Rubella signs and symptoms, post natal
malaise, mild fever, sore throat ad lymphadenopathy. A rash of pink macules and papules first appears on the face and progresses down the trunk and toward the extremities, advancing and resolving in ~3 days. In adults, the infection is often accompanied by joint inflammation and pain rather than rash.
Rubella signs and symptoms congenital
Rubella is teratogenic virus and can cause congenital defects in the fetus. Defects depend on when the fetus is exposed in utero. In the 1st trimester it is likely to cause miscarriage or multiple permanent defects. The most common is deafness. Others are cardiac abnormalities, ocular lesions, mental and physical retardation. Complications that usually resolve in time are anemia, hepatitis, pneumonia, carditis, and bone infections.
Rubella prevention
MMR vaccine
papillomas, are benign, squamous epithelial growths. They can infect mucous membranes or invade skin. Rarely, a wart can become malignant when caused by a particular type of HPV.
Warts causative agent
Human papillomaviruses, common warts (Found on fingers and other parts of the body) are often caused by HPV 2, 4, 27, 29. Planter warts (deep painful papillomas on the soles of the feet) are caused by HPV 1. Flat warts (smooth, skin-colored lesions that develop on the face, trunk, elbows and knee) are caused by HPV 3, 10, 28, 49
Warts transmission
direct contact, autoinoculation, indirect contact.
Warts treatment
home remedies (OTC-salicyclic acid preps, adhesive tape) cryosurgery, no guarantee that the virus is eliminated
Cutaneous anthrax
The most common and least dangerous form of Bacillus anthracis
Cutaneou anthrax--causative agent
Bacillus anthracis
Cutaneous anthrax--signs and symptoms
Germination and growth of the pathogen in the skin are marked by the production of a papule that becomes increasingly necrotic and later ruptures to form a painless, black eschar.
Cutaneous anthrax--transmission
direct contact with endospore
Cutaneous anthrax-treatment
Ciproflaxicin, doxycycline, penicillin
Cutaneous mycoses
Caused by a group of fungi collectively called dermatophytes causes mycoses that are confined to the nonliving epidermal tissues, hair and nails. These diseases are often called “ringworm.”
Cutaneous mycoses--causative agents
Genera Trichophyton, Microsporum, Epidermophyton
Cutaneous mycoses--areas that can be affected
scalp, beard, body, hand, and nail
Cutaneous mycoses--virulence factors
Ability to degrade keratin, and invoke hypersensitivity
Cutaneous mycoses treatment
topical tolnaftate, itraconazole, terbinafine miconzaole, thiabendazole
Infection of the conjunctiva, commonly called pink eye has many different clinical presentations, highly contagious
Conjunctivitis causative agents
Neonatal (in babies less an 28 days)—Neisseria gonorrhoeae or Chlamydia trachomatis (usually transmitted vertically from the mother) Other age groups—commonly caused by Staphylococcus epidermidis, Streptococcus pyogenes, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella species. In adults, N. gonorrhoeae and C. trachomatis (autoinoculation) Other bacteria, fungi, protozoa from contaminated contact lessen, lens cases, and contact solution (vehicle transmission)
conjunctivitis signs and symptoms
Bacterial infections—milky discharge; viral infections—clear exudate. Pain is generally mild, at times gritty sensation; redness and eyelids swelling are common, photophobia at times
Conjunctivits transmission
Neonatal—vertical; Bacterial—direct, indirect contact; viral—direct, indirect contact
Conjunctivitis prevention
good hygiene is the only way to prevent conjunctivitis in adults and children other than neonates. Newborn children in the US are administered antimicrobials in their eyes after delivery to prevent neonate conjunctivitis from either N, gonorrhoeae, or C. trachomatis.
Conjunctivitis treatment
Neonatal—topical and oral antibiotics; Bacterial—broad spectrum topical antibiotic, often ciprofloxacin; Viral—none although antibiotics given because type of infection is not distinguished
A more serious eye infection than conjunctivitis, invasion of deeper eye tissues occurs and can lead to complete corneal destruction. Viral condition is leading infectious cause of blindness in the US
Keratitis causative agent
Herpes simplex virus type 1 (oral) and miscellaneous microbes
Keratitis--signs and symptoms
gritty feeling, conjunctivitis, sharp pain, sensitivity to light
Keratitis pathogenesis
Latency—misdirected reactivation—the oral HSV-1 travels into the ophthalmic rather than the mandibular branch of the trigeminal nerve
Keratitis Transmission
Reactivation of the latent virus, although primary infections can occur in the eye, often traumatic introduction (parental)
Keratitis treatment
topical vidarabine and/or oral acyclovir for HSV-1, specific antimicrobials for miscellaneous microbes
Meningitis is an inflammation of the meninges. Many different microbes can cause it, but the signs and symptoms are similar
Meningitis signs and symptoms
1) Headache 2) Painful or stiff neck 3) Fever 4) Increase in number of white blood cells in cerebrospinal fluid (CSF) 5) Convulsions 6) Vomiting Increase protein and decrease glucose happens in bacteria. Increase in phagocytic cells. Viral—increase protein and increases lymphocytes. 7) Swelling of the brain tissue, infarct (tissue death, brain tissue) 8) CSF Circular obstruction—build up of pressure. 9) Damage to nerves that are essential for hearing, vision, or motor nerves.
Meningitis causative bacterial agents
Neisseria meningitidis a gram negative diplococci, also known as meningococcus
Neisseria meningitidis
most serious form, associated with epidemic forms...its is responsible for 25% of all meninigitis cases
Pathogenesis of Neisseria meningitidis-
Rapid progress, death can occur in hours. 1) Capsules 2)Endotoxin—the Endotoxin released by meningococcus which stimulated white blood cells. This causes meningococcemia in which the WBCs release cytokines which leads to vascular collapse, hemorrhage and lesions called petechiae on the trunk and appendages. If meningococcemia becomes fulminant, a high mortality rate accompanies it. Meningococcemia has a sudden onset, a high fever (40°), delirium, severe widespread ecchymosis (bleeding under the skin), shock and coma. Generalized intravascular clotting, cardiac failure, damage to the adrenal glands and death can occur within a few hours. 3)IgA protease—break down IgA.
Neisseria meningitidis transmission
Transmitted by close contact with secretions or droplets. It has sporadic or epidemic incidence in late winter or early spring. The reservoir is humans carrying the pathogen in the nasopharynx. The carrier state can last from a few days to several months and exists in 3% to 30% of adult population, but can exceed 50% in institutional settings. Schools, colleges, long term care facilities, jails. The highest risk groups are young children (6 to 36 months old) and older children and young adults (10 to 20 years old). Haven’t developed immunity.
Neisseria meningitidis prevention
Infection rate is ~1%, so there is a well developed immunity to meningococcus. Conjugate vaccine—2005 type A, C, Y and W135. Recommended for college and high school students. Resistance is due to poisoning antibodies against the capsular polysaccharides and membrane antigens. Prophylactic treatment with rifampin or tetracycline is used in cases of contact. No vaccine for Strain B—prophylactic treatment is necessary. Meningococcal vaccines are available to high risk groups.
Neisseria meningitidis--treatment
The mortality rate for treated meningoccemial disease 15%, so treatment has to begin as soon as possible with one or more drugs. Penicillin G is the most potent drug against meningococcal infections, and is usually given in high IV doses.
Streptococcus pneumoniae--small gram positive cocci in pairs
Most frequent cause of community acquired meningitis. Most common cause of adult meningitis
Strep pneumoniae--meningitis--pathogenesis
Capsules, induction of apoptosis (cell death), hemolysin and hydrogen peroxide production
Strep pneumoniae--prevention
Two vaccines are available, Prevnar for children and Pneumovax for adults.
Strep pneumoniae--treatment
Drug susceptibilities must be tested. Ceftriaxone is used often, and because of resistance, penicillin is usually ruled out.
Haemophilus influenzae
Type B responsible for most of the cases
Mortality rare
Haemophilus influenzae--transmission
Transmitted via droplet contact, and not associated with epidemics, but sporadic outbreaks in day cares and family settings. Healthy adult carriers are the usual reservoirs. The number of cases has declined because of vaccination
Haemophilus influenzae--prevention
Routine vaccination is recommended for all children beginning at 2 months with 3 follow up boosters
Haemophilus influenzae treatment
Usually treated with ceftriaxone, prophylaxis with rifampin for contacts
Listeria Monocytogenes
is a gram positive bacilli that is not fastidious and is resistant to cold, heat, pH extremes and bile
Listeria Monocytogenes signs and symptoms
In normal adults it is a mild or subclinical infection with nonspecific symptoms of fever, diarrhea and sore throat. In elderly, immunocompromised patients, fetuses and neonates, listeriosis usually affects the brain and meninges and result in septicemia.
Listeria monocytogenes transmission
Transmission is usually via food products, but it can be transmitted to an infant either prenatally across the placenta or postnatally via the birth canal. It has been isolated from ground beef, chicken, turkey, luncheon meats, hot dogs and cheeses. Cheeses made from raw milk (unpasteurized) are of special concern.
Listeria monocytogenes prevention
Adequate pasteurization temperatures, proper washing, refrigeration, and cooking of food. Pregnant women are cautioned not to eat soft, un-pasteurized cheese.
Listeria monocytogenes treatment
Drugs of choice are ampicillin and trimethoprim—sulfamethoxazole, followed by erythromycin. Treatment should be started as soon as listeriosis is suspected.
Crytococcus neoformans
is a yeast that causes a more chronic form of meningitis with a more gradual onset of symptoms. The primary ecological niche is the bird population. It is a spherical to ovoid shape with small, constricted buds and a large capsule. 1975—Filobasdilla neoformans
Cryptococcus neoformans culture and diagnosis
Capsule stain (India ink or negative staining), culture, biochemical test, DNA probes.
Cryptococcus neoformans pathogenesis
Capsules, affinity for the meninges and brain. The yeast forms tumor-like masses in the meninges and brain that can cause headaches, mental changes, coma, paralysis, eye disturbances and seizures.
Cryptococcus neoformans treatment
Immediate treatment with amphotericin B and Fluconazole over a period of weeks or months. There are no preventative measures.
i. Enteroviruses—90%
ii. Herpes viruses
iii. Arboviruses
iv. Arenaviruses
v. Adenoviruses
vi. HIV
Viral culture and diagnosis
Absence of bacteria, fungi, or protozoa in CSF, followed by viral culture or antigen tests. Increase lymphocytes, CSF glucose level is going to remain within the normal range.
Viral transmission and epidemiology
Droplet contact—starts in the throat or intestines—moves to bloodstream -->CNS
viral treatment
Viral meningitis is generally milder than bacterial or fungal meningitis and usually resolves within 2 weeks without treatment. Acyclovir can be used when a herpesvirus is the causative agent and the HIV regimen is used when HIV is the causative agent.
neonatal causative agents
i. Streptococcus agalactiae (Beta Strep Group B)—it colonizes 10% to 30% of female genital tracts and the most frequent cause of neonatal meningitis.
Neonatal causative---E. Coli
the second most common cause of neonatal meningitis. Most babies suffer from this infection are premature and their prognosis is poor.
Neonatal cause
Listeria monocytogenes--is a gram positive bacilli that is not fastidious and is resistant to cold, heat, pH extremes and bile
Neonatal transmission
Strep—vertical during birth E. coli—strain K1—vertical during birth. Listeria—vertical ether prenatally or during birth.
Neonatal prevention
Strep—culture and treatment of mother E. coli—strain K1?? Listeria—cooking food, avoiding unpasteurized dairy products
Neonatal treatment
Penicillin G plus Aminoglycosides E. coli—Ceftriaxone plus Aminoglycosides Listeria—Ampicillin, trimethoprim-sulfamethoxazole
Acute Encephalitis
Is usually caused by viruses. It is a serious condition because the tissues of the brain are very sensitive to the inflammatory processes
Acute Encephalitis causative agents
1.arboviruses—which include the causative agents of the Western Equine Encephalitis (WEE), Eastern Equine Encephalitis (EEE), California Encephalitis, St. Louis Encephalitis (SLE), and West Nile Encephalitis (WN). Can also be caused by Herpes Simplex virus type 1 and 2, JC virus (a polyoma virus).
2. herpes virus
3. JC virus
acute encephalitis transmission
1. general route (you don’t need to know the exact route for each) Western equine encephalitis-sporadic occurrences in the western U.S. and Canada in early summer. Very dangerous to infants and small children with a mortality rate of 3% to 7%. Eastern Equine encephalitis—endemic along the eastern coast of North America and Canada with sporadic pattern and occasional endemics. Mortality rate can be up to 70%. California encephalitis—caused by two viral strains, the California strain occurs occasionally in the western US and has little impact on humans. The LaCrosse strain is widely distributed in the eastern US and Canada. It is the prevalent cause of viral encephalitis in North America. Primary target group are children in rural areas with mild transient symptoms and fatalities are rare. St Louis encephalitis—most common, cases appear throughout North and South America, U.S. epidemics in the Midwest and South. Peak seasons are spring and summer depending on region and species of mosquito. West Nile encephalitis—a close relative of the SLE Illness usually is characterized by flu-like symptoms, <1% infected persons will suffer lethal inflammation. Herpes Simplex Virus—vertical transmission from mother to newborn. Virus is disseminated and prognosis is poor. Reactivation of latent virus in the trigeminal ganglion is the cause in older children and young adults (ages 5 to 30) and older adults (over 50). Other virus-associated Encephalitis—Post Infection Encephalitis (PIE) can occur 1 or 2 weeks after infection with one of the childhood rash diseases. It is believed to be related to an inappropriate immune response and not viral invasion of the CNS.
acute encephalitis treatment
For arboviruses—none; for herpes simplex 1 or 2—acyclovir, for JCV-zidovudinez or other antivirals; for other virus-associated encephalides—steroids, anti-inflammatory agents
Subactue encephalitis
When encephalitis symptoms take longer to present and are less striking, the condition is called subacute encephalitis. The most common causes follow
Subacute enceph Toxoplasma gondii
is a flagellated parasite with worldwide distribution. In most cases, the infection goes unnoticed, but in the fetus and Immunodeficient patients it is severe and often fatal.
Subacute enceph signs and sytmptoms Toxoplasma gondii
asymptomatic or mild symptoms including sore throat, lymph node enlargement, and low grade fever. In immunocompromised patients, the infection causes a more chronic or subacute form producing extensive brain lesions and fatal disruptions of the heart and lungs. A pregnant women with toxoplasmosis has a 33% chance of transmitting it to her fetus. Congenital infection occurring in the 1st of 2nd trimester cause stillbirth of severe abnormalities including liver and spleen enlargement, liver failure, hydrocephalus, convulsions, and retinal damage.
Subacute enceph transmission of toxoplasma gondii
fecal-oral transmissions or by eating contaminated meat. Taxoplasma gondii has a large animal reservoir that becomes infected through contact with oocysts in the soil. Humans can be infected through contact with cats or ingestion of pseudocysts in animal flesh.
subacte enceph prevention toxoplasma gondii
good personal and food hygiene. Pregnant women should never clean a cat’s litter box.
subacute encep toxoplasma gondii treatment
Most effective drugs are pyrimethamine and sulfadiazine alone or in combination. These don’t destroy the cyst stage, so they must be given for long periods.
Subacute sclerosing panencephalitis causative agent
Measles virus, years after the initial measles infection
Subacute sclerosing panencephalitis signs and symptoms
encephalitis with history of measles.
Subacute sclerosing panencephalitis transmission
Persistence of measles virus
Subacute sclerosing panencephalitis treatment
no treatment
are proteinaceous infectious particles containing no genetic material. They cause diseases called transmissible spongiform encephalopathies. (TSE). TSEs are neurodegenerative diseases with long incubation periods but rapid progressions once they begin. The human TSEs are Creutzfeldt-Jakob disease (CJD), Gerstmann-Strussler-Scheinker disease and fatal familial insomnia. Bovine spongiform encephalopathy (BSE) is commonly known as mad cow disease and has an apparent link to a variant form of CJD. vCJD=mad code disease.
Prions main characterisitics
1) Increase in quantity during incubation period. 2) Resist inactivation by ultraviolet and ionizing radiation. 3) Resist inactivation by formaldehyde and heat. 4) Not readily destroyed by proteases. 5) Not destroyed by nucleases. 6) Smaller than the smallest virus. 7) Composed of protein coded by a normal cellular gene, but modified after transcription.
Prions signs and symptoms
CJD symptoms include altered behavior, dementia memory loss, impaired senses, delirium and premature senility. Uncontrollable muscle contractions
Prions transmission
CJD is not communicable with oridinary contact with infected people. Direct or indirect contact with infected brain tissue or CSF may result in prion transmission. Classic presentation a proportion of the cases are transmitted, and other cases appear to be inherited. Classic presentationsoccur at a rate of 1 case per million persons and the mediate age at death is 68 years.
Prions treatment
No known treatment exists for either form of CJD. Medical intervention focuses on easing symptoms and making the patient as comfortable as possible.
is a slow, progressive zoonotic disease characterized by fatal encephalitis. It is very distinctive in its pathogenesis and symptoms. It is distributed nearly worldwide except for 34 countries that have remained rabies-free by practicing rigorous animal control.
Rabies causative agent
rabies virus is in the family Rhabdoviridiae, genus Lyssavirus. The rabies virus particles have a distinctive bullet like appearance, round at one end and flat on the other. It has a helical nucleocapsid and spikes that protrude through the envelope.
Rabies signs and symptoms
Average incubation time 1 to 2 months or more depending on the wound site, severity and inoculation dose. The incubation period is shorter in facial, scalp or neck wounds because of closer proximity to the brain. The prodromal phase begins with fever, nausea, vomiting, headache, and fatigue.
rabies forms
There are two forms: 1) Furious form—first acute signs of neurological involvement are periods of agitation, disorientation, seizures, and twitching. Spasms in neck and pharyngeal muscles lead to severe pain upon swallowing leading to hydrophobia symptom. The patient is fully coherent and alert during this phase. 2) Dumb form, the patient is paralyzed, disoriented, and stuporous. Both forms progress to the coma phase and death resulting from cardiac or respiratory arrest.
Rabies pathogenesis
Infection begins with the infected animal’s saliva entering a puncture site. The virus remains in the wound for up to a week and multiplies; it enters the nerve endings and moves toward the ganglia, spinal cord and brain. After multiplication in the brain is then followed by migration to the eyes, heart, skin, and oral cavity. Rabies virulence is associated with an envelope glycoprotein that gives the virus its ability to spread in the CNS and invade neural cells.
Rabies transmission
Primary reservoirs are wild mammals such as canines, skunk, raccoons, badges, cats and bats that can spread the infection to domestic dogs and cats. Both wild and domestic mammals can spread the disease to humans through bites, scratches, and inhalation of droplets.
Rabies prevention
Vaccination of domestic animals, elimination of strays, and strict quarantine practices. For high risk human groups, (veterinarians, animal handlers, etc.) three doses of vaccine should be given.
Rabies treatment
After an animal bite, the would should be meticulously cleaned with soap and water, followed by debridement and application of an antiseptic. The wound is infused with human rabies immune globulin (HRIG) and globulin is also injected intramuscularly. A full course of vaccination is started at the same time, intramuscular or intradermal injection the 1st, 3rd, 7th, 14th, 28th, and 60th days, then two additional boosters.
is an acute enteroviral infection of the spinal cord that can cause neuromuscular paralysis. If often affects small children, so it used to be called infantile paralysis. The number of cases worldwide have been drastically reduced and WHO (World Health Organization) is moving toward eradication of all remaining wild polioviruses.
Poliomyelitis causative agent
poliovirus is in the family Picornaviridae, genus Enterovirus. It is nonenveloped and nonsegmented, the naked capsid of the virus confers chemical stability and resistance to acid, bile and detergents
Poliomyelitis signs and symptoms
most infections are short-termed, mild viremias. Some develop mild nonspecific symptoms of fever, headache, nausea, sore throat, and myalgia. If viremia persists, the virus is carried to the CNS via the blood and spreads in the spinal cord and brain. Non-paralytic disease involves the invasion but not the destruction of nerve tissue and cause muscle pain and spas, meningeal inflammation and vague hypersensitivity. Paralytic diseases invasion of the motor neurons causes various degrees of flaccid paralysis over a period of a few hours to several days. Depending on the level of damage to motor neurons, paralysis of the muscles of the legs, abdomen, back, intercostals, diaphragm, pectoral girdle and bladder can result. In rare cases of bulbar poliomyelitis, the brain stem, medulla or cranial nerves
Poliomyelitis diagnosis
viral culture and serology
Poliomyelitis pathogenesis
the virus is ingested and carried to the throat and intestinal mucosa. The virus multiplies in the tonsils and escapes to the lymph nodes and blood. The viruses are further amplified and cross into the nerve cells of the CNS. The intestine actively sheds the virus.
is a neuromuscular disease also called lockjaw
Tetanus causative agent
Clostridum tetani is an anaerobic gram-positive, spore forming bacillus. It is normally found in soil and the gastrointestinal tracts of animals. Generally localized infection
Tetanus symptoms
Early symptoms include restlessness, irritability, difficulty swallowing, contraction of muscles, and sometimes convulsions. C. tetani release the neurotoxin, tetanospasmin, which binds to target sites on spinal neurons and blocks the inhibition of muscle contractions, without the inhibition, muscles contract uncontrollably. The first symptoms are clenching of the jaw, followed in succession by extreme arching of the back, flexion of the arms and extension of the legs. Death occurs due to paralysis of the respiratory muscles and respiratory arrest.
Tetanus transmission
spores usually enter the body through accidental puncture wounds, burns, umbilical stumps, frostbite, and crush injuries. Incidence is low in North America with the most cases seen in geriatric patients and IV drug abusers
Tetanus prevention
Tetanus toxic immunization
Tetanus treatment
If the clinical picture suggest tetanus; antitoxin is administered to inactivate the circulating toxin. This will not counteract the effect of the toxin already bound to neurons. Other treatments include cleansing and removing infected tissue, controlling the infection with penicillin or tetracycline and the administration of muscle relaxant.
is often an intoxication rather than infection and is associated with poorly preserved foods. There are three major forms: food borne (children and adults) infant, tied to honey ingestion, and wound.
Botulism causative agent
an anaerobic spore-forming, gram positive bacillus. That releases an exotoxin, botulin. It is commonly found in soil and water and occasionally in the GI tract of animals. It is distributed worldwide, but occurs most often in the Northern Hemisphere. Exotoxin is one of the most powerful poisons known, a few mg could kill the whole population of a large city
Poliomyelitis symptoms
most infections are short-termed, mild viremias. Some develop mild nonspecific symptoms of fever, headache, nausea, sore throat, and myalgia. If viremia persists, the virus is carried to the CNS via the blood and spreads in the spinal cord and brain. Non-paralytic disease involves the invasion but not the destruction of nerve tissue and cause muscle pain and spas, meningeal inflammation and vague hypersensitivity. Paralytic diseases invasion of the motor neurons causes various degrees of flaccid paralysis over a period of a few hours to several days. Depending on the level of damage to motor neurons, paralysis of the muscles of the legs, abdomen, back, intercostals, diaphragm, pectoral girdle and bladder can result. In rare cases of bulbar poliomyelitis, the brain stem, medulla or cranial nerves
Poliomyeltis pathogenesis
the virus is ingested and carried to the throat and intestinal mucosa. The virus multiplies in the tonsils and escapes to the lymph nodes and blood. The viruses are further amplified and cross into the nerve cells of the CNS. The intestine actively sheds the virus.
Tetanus signs and symptoms
Early symptoms include restlessness, irritability, difficulty swallowing, contraction of muscles, and sometimes convulsions. C. tetani release the neurotoxin, tetanospasmin, which binds to target sites on spinal neurons and blocks the inhibition of muscle contractions, without the inhibition, muscles contract uncontrollably. The first symptoms are clenching of the jaw, followed in succession by extreme arching of the back, flexion of the arms and extension of the legs. Death occurs due to paralysis of the respiratory muscles and respiratory arrest.
Tetnaus prevention
tetanus toxic immunization
Botulism signs and symptoms
the symptoms are the same for all three forms. The toxin travels from the circulatory system to the neuromuscular junctions of skeletal muscles. Botulin prevents the release of neurotransmitter, acetylcholine, which initiates the signal for muscle contraction. Neuromuscular symptoms include double vision, difficulty swallowing and dizziness. Later symptoms are descending muscular paralysis and resipiratory arrest, use of ventilators has reduced mortality rates to 10%. Symptoms occur in 12 to 36 hours after ingesting the contaminated food.
Botulism pathogenesis
the exotoxin botulin
Botulism transmission
vehicle (food borne toxin, airborne organism); direct contact (wound) parental (injection)
Botulism prevention
food hygiene; toxoid immunization available for laboratory professionals Toxin is also heat labile.
Botulism treatment
antitoxin will only neutralize toxin circulating in the blood, not the toxin already bound to nerve cells, supportive care.
Physical barrier
the skin and mucous membranes of the respiratory and digestive tracts have several built-in defenses. The outermost layer (stratum corneum) of the skin is composed of epithelial cells that have become compacted, cemented together, and impregnated with an insoluble protein, keratin
Chemical Barrier
Sebaceous secretions exert an antimicrobial effect, and specialized glands such as the meibomian glands of the eyelids lubricate the conjunctiva with an antimicrobial secretion. An additional defense in tears and saliva is lysozyme, an enzyme that hydrolyzes the Peptidoglycan in the cell wall of bacteria.
Genetic Barrier
One explanation for this phenomenon is that some pathogens have such great specificity for one host species that they are incapable for infecting other species. One way of putting it is “Humans can’t acquire distemper from cats, and cats can’t get mumps from humans.”
Innate or nonspecific
Inflammatory Response is a reaction to any traumatic event in the tissues. It is common-place that most of us manifest inflammation in some way everyday. It is readily identifiable by a classic series of signs and symptoms of allergy. It is readily identifiable by rubor (redness), calor (warmth), tumor (swelling) and dolor (pain)
1) Mobilize and attract immune components to the site of the injury 2) to set in motion mechanisms to repair tissue damage and localize and clear away harmful substances 3) destroy microbes and block their further invasion.
represent an impressive piece of living machinery, meandering through the tissues to seek, capture, and destroy a target. The general activities are: 1) To survey the tissue compartments and discover microbes, particulate matter (dust, carbon particles, antigen-antibody complexes), and injured or dead cells; 2) to ingest and eliminate these materials; and 3) to extract immunogenic information (antigens) from foreign matter.
Types of phagocytes
neutrophils, monocytes, and macrophages.
a small protein produced naturally by certain white blood and tissue cell that is used in therapy against certain viral infections and cancer. All three classes of interferon are produced in response to viruses, RNA, immune products, and various antigens. Their biological activities are extensive. In all cases, they bind to cells surfaces and induce changes in genetic expression, but the exact results vary.
is brought into play at several levels. The complement system consists of at least 26 blood proteins that work in concert to destroy bacteria and certain viruses.
Naturally acquired
encompasses any immunity that is acquired during the normal biological experiences of an individual rather than through medical intervention
encompasses any immunity that is acquired during the normal biological experiences of an individual rather than through medical intervention
occurs only as a result of the prenatal and postnatal, mother-child relationship. During fetal life, IgG antibodies circulating in the maternal bloodstream are small enough to pass or be actively transported across the placenta. Antibodies against tetanus, diphtheria, pertussis, and several viruses regularly cross the placenta. This natural mechanism provides and infant with a mixture of many maternal antibodies that can protect it for the first few critical months outside the womb, while its own immune system is gradually developing active immunity.
Artificially acquired
is protection from infection obtained through medical procedures. This type of immunity is induced by immunization with vaccines and immune serum.
artifical active
the term vaccination originated from the Latin word vacca (cow) because the cowpox virus was used in the first preparation for active immunization against small pox. Vaccination exposes a person to a specially prepared microbial (antigenic) stimulus, which then triggers the immune system to produce antibodies and lymphocytes to protect the serum upon further exposure to that microbe. As with natural active immunity, the degree and length of protection vary. Commercial vaccines are currently available for many diseases.
passive artificial
In immunotherapy, a patient at risk for acquiring a particular infection is administrated a preparation that contains specific antibodies against that infectious agent. In the past, these therapeutic substances were obtained by vaccinating animals, then taking blood and extracting the serum. Pooled human serum from donor blood and immune serum globulins containing high quantities of antibodies are more frequently used. Immune serum globulins are used to protect people who have exposed to hepatitis, measles, and rubella. More specific immune serum obtained from patients recovering from a recent infection, is useful in preventing and treating hepatitis B, rabies, pertussis, and tetanus.
Mechanism of Phagocytosis
Phagocytes often trap cells or debris against the fibrous network of connective tissue or debris against the fibrous network of connective tissue or the wall of blood and lymphatic vessels. Once the phagocyte has made contact with its prey, it extends pseudopods that enclose the cells or particles in a pocket and internalize them in a vacuole called a phagosome. It also secretes more cytokines to further amplify the innate response.
a chemical substance produced by white blood cells and tissue cells that regulates development, inflammation, and immunity
Antigen presentation
Three different cells can serve as APCs: macrophages, B cells, and dendritic cells. Dendritic cells engulf the antigen and modify it so that it will be more immunogenic and recognizable to lymphocytes. After processing is complete, the antigen is moved to the surface of the APC and bound to the MHC (Major Histocompatibility Complex) receptor so that it will be readily accessible to the lymphocytes during presentation.
the progeny of a dividing B-cell clone or called plasma cells. These cells are programmed to synthesize and secrete antibodies into the tissue fluid and blood. When these antibodies attach to the antigen for which they are specific, the antigen is marked for destruction or neutralization. Because secreted antibody molecules secreted circulate feely in the tissue fluids, lymph, and blood, the immunity they provide is humoral.
T cell receptors
bind processed antigens plus MHC molecules on the cells that present antigens to them. The t-cell receptor for antigen belongs to the same protein family as the B-cell receptor. Unlike immunoglobulins, the T-cell receptor is relatively small and is never secreted.
Major Histocompatibility molecules
One set of genes that codes for human cell receptors is the major histocompatibility complex. The MHC is also known as the human leukocyte antigen system. This receptor complex plays a vital role in recognition of self by the immune system and in rejection of foreign tissue. Class 1 genes code for markers that display unique characteristics of self and allow for the recognition of self molecules and the regulation of immune reactions. Class 2 MHC genes also code for immune regulatory receptors are found on macrophages, dendritic T cells during cooperative immune reactions.
B Cell activation
becomes activated when it finds an antigen and binds to it. Once a helper T cell has been activated by an antigen, it becomes capable of activating a B cell that has already encountered the same antigen
T cell activation
T cell types and responses are extremely varied. When activated (sensitized) by antigen, a T cell gives rise to one of the three different types of progeny, each involved in a cell-mediated immune function. The three main functional types of T cells are: 1) Th1 that activate the CMI pathway 2) Th2 cells that assist B-cell processes 3) TC cells that lead to the destruction of infected host cells and other “foreign” cells. They do not produce antibodies.
lobed nuclei and their fine pale lavender granules. 55%-90% of the circulating neutrophils. The main work is phagocytosis.
blood phagocytes that rapidly leave the circulation mature into macrophages
Lymphocyte b cells
differentiate into plasma cells and form antibodies (humoral antibodies)
Lymphocyte T cells
perform a number of specific cellular immune responses such as assisting B cells and killing foreign cells (cell-mediated immunity)
Mast cells
specialized tissue cells similar to basophiles that trigger local inflammatory reactions and are responsible for many allergic symptoms
Dendritic cells
Relatives of macrophages that reside throughout the tissues and RES; responsible for processing foreign matter and presenting it to lymphocytes.
the body temperature is normally maintained by a control center in the hypothalamus region of the brain. Fever is initiated when a circulating substance called pyrogen resets the hypothalamic thermostat to a higher setting. This change signals the musculature to increase heat production and peripheral arterioles to decrease heat loss through vasoconstriction.
infiltration of site by neutrophils and accumulation of pus
either by complete resolution and return of tissue to normal state or by formation of scar tissue.
Traits that can be assessed with the naked eye are also useful in diagnosis. These include the appearance of colonies, including texture, size, shape, pigment, speed of growth, and patterns of growth in broth in gelatin media.
Traits that can be valuable aids to identification are combinations of cell shape and size, gram stain reaction, acid-fast reaction, and special structures, including endospores, granules, and capsules.
Biological testing
These have been the traditional mainstay of bacterial identification. Enzymes and other biochemical properties of bacteria are fairly reliable and stable expressions of the chemical identity of each species. Dozens of diagnostic tests exist for determining the presence of specific enzymes and to assess nutritional and metabolic activities.
DNA analysis
The exact order and arrangement of the DNA code is unique to each organism. With a technique called hybridization, it is possible to identify a bacterial species by analyzing segments of its DNA. This requires small fragments of single-stranded DNA (or RNA) called probes that are known to be complementary to the specific sequences of DNA from a particular microbe
Nucleic acid sequencing/ rRNA analysis
One of the most viable indicators of evolutionary relatedness and affiliation is comparison of the sequence of nitrogen bases in ribosomal RNA, a major component of ribosomes. Ribosomes have the same function (protein synthesis) in all cells, and they tend to remain more or less stable in their nucleic acid content over long periods. Thus, any major differences in the sequence, or “signature” of the rRNA is likely to indicate some distance in ancestry. This technique is powerful at two levels: it is effective for differentiating general group differences and it can be fine tuned to identify at the species level.
Polymerase chain reaction
Many nucleic acid assays use the polymerase chain reaction (PCR). This method can amplify DNA present in samples even in tiny amounts, which greatly improves the sensitivity of the test. PCR tests are being used or developed for a wide variety of bacteria, viruses, protozoa, and fungi.
Serological test
Serology is the branch of immunology that traditionally deals with in vitro diagnostic testing of serum. Serological testing is based on the familiar concept that antibodies have extreme specificity for antigens, so when a particular antigen is exposed to its specific antibody, it will fit like a hand in a glove. The basis of serological tests is that Abs specifically binds to Ag in vitro. An Ag of known identity will react with antibodies in an unknown serum sample. The reverse is also true; known antibodies can be used to detect and type antigens
is the property of a test to focus on only a certain antibody or antigen and will not react with unrelated or distantly related ones.
means that the test can detect even very small
amounts of antibodies or antigens that are the targets of the test
Microscopic tests
a. gram stain
b. acid fast stain
c. Fluorescent Ab stain— An unknown test specimen or antigen is fixed to a slide and exposed to a fluorescent antibody solution of known composition. If the antibodies are complementary to antigens in the material, they will bind to it. After the slide is rinsed to remove unattached antibodies, it is observed with the fluorescent microscope. Fluorescing cells or specks indicate the presence of Ab-Ag complexes and a positive result.
Macroscopic--direct antigen
a technique similar to direct fluorescence in that known antibodies are used to identify antigens on the surface of bacterial isolates. But in direct antigen testing, the reactions can bee seen with the naked eye. Quick test kits that greatly speed clinical diagnosis are available for Staphylococcus aureus, Streptococcus pyogens, Neisseria gonorrhoeae, Haemophilus influenzae, and Neisseria meningitidis however, when the microbe is very sparse in the specimen, direct testing is like looking for needle in a hay stack.
animal inoculation
animals must be inoculated to cultivate bacteria such as Mycobaterium leprae and Treponema pallidum, whereas avian embryos and cell cultures are used to test bacterial or fungal virulence.
In vivo testing
Tuberculin test—uses a small amount of purified protein derivative from Mycobacterium tuberculosis injected into the skin. The appearance of a red, raised, thickened lesion in 48-72 hours can indicated a previous exposure to tuberculosis.
Anatomy of skin
the skin, together wit the hair, nails and sweat and oil gland from the integument. The skin has a total surface area of 1.5 to 2 square meters. Its thickness varies from 1.5 mm at places such as the eyelids and 4mm on the soles of the feet. The outermost portion of the skin is the epidermis, which is dived into 4-5 more layers. No nerve endings or blood vessels in the stratum corneum or any other portion of the epidermis. The lowest layer, the stratum basale, or basal layer is attached to the underlying dermis and is the source of all the cells that make up the epidermis. The dermis underneath the epidermis, is composed of connective tissue instead of epithelium. The skin is brimming with antimicrobial substances.
Epidermis keratin
On top is a thick layer of epithelial cells called the stratum corneum, about 25 cells thick. The cells in this layer are dead and have migrated from the deep layers during the normal course of cell division. They are packed with a protein called keratin.
gives the cells their ability to withstand damage, abrasion, and water penetration, the surface of the skin is termed keratinized for this reason.

Add Cards

You must Login or Register to add cards