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UT / Biology / BIOL 210 / how genital warts transmit?

how genital warts transmit?

how genital warts transmit?

Description

School: University of Tennessee - Knoxville
Department: Biology
Course: Microbiology
Professor: Elizabeth mcpherson
Term: Fall 2015
Tags: Microbiology
Cost: 50
Name: Microbiology Final Study Guide
Description: This is a chart with all the information we need to know about all of the categories of infectious diseases we learned about in this unit. Good luck on the final!
Uploaded: 05/04/2016
7 Pages 13 Views 17 Unlocks
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Skin infections Folliculitis Rocky Mountain Spotted Fever


how genital warts transmit?



Chicken Pox /

Shingles Measles

Causative Agent

Staphylococcus  

(epidermis or aureus)

Rickettsia rickettsii

Varicella-Zoster virus

Rubeola

Organism Characteristics

Gram+ cocci that collect in a  ‘grape cluster’ formation

Intracellular, Gram-,  

coccobacillus

Icosahedral, enveloped, DNA

Helical nucleocapsid, envelope,  ssRNA

Reservoir

Mucous membranes, skin

Rodents (zoonosis)

Other people, highly infectious

People, highly contagious

Mode of Transmission

Direct contact and fomites

Biological vector: ticks

Respiratory droplets and direct  contact through lesion fluid

Respiratory droplets

Portal of Entry

Sebaceous gland of hair follicle

Parenteral

Respiratory tract

Back of the throat

Organism’s Virulence


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Factors

Only aureus is virulent:  

coagulase, hyaluronidase,  staphyloskinase, lipases, Protein  A, slime layer

Not killed by host cells

Latency, envelope, DNA

Hemagglutinin (attachment)  and viral fusion protein to enter  cells and force membrane  fusion with other cells

How Organism Affects Body

forms pimple, sty (edge of  eyelid), furuncle (boils), or  carbuncle (escalation of  

furuncle)

Causes damage to blood cells  which results in loss of fluid,  low blood volume, reduced flow  to organs, disordered tissue  function and thrombocytopenia

Temporary vision problems,  hearing loss, paralysis of face,  ongoing pain

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Signs and Symptoms

Red, swollen pustules show up  at the area of infection

Non-itchy, spotted rash and  petechiae


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Fever, lesions covering the body  form papules which then scab  over and fall off

Fever, sore throat, dry cough,  conjunctivitis, Koplik spots,  raised lesions/rash on skin

Sequelae

Scarring, may develop into  MRSA (if the strain doesn’t  respond to antibiotics)

Respiratory, CNA, GI, and renal  system failure, encephalitis, and  death

Development of Shingles later  in life. Tissue damage as a result  of the immune response

Secondary infections common,  more severe the second time

Epidemiology

S. epidermis is part of normal  flora, and S. aureus is very  common as well

Common in Appalachia,  

Oklahoma, and the  

southeastern US

Highly contagious. Seen in  children mostly, is more severe  in adults

Very contagious. Infants,  pregnant women,  

immunocompromised people

Diagnosis

Positive coagulase test points to  virulent S. aureus infection,  while negative indicates  

opportunistic S. epidermis

Rash on palms and soles,  sudden fever, headache  

following exposure to ticks

Tell-tale lesions and

Via signs. Koplik spots in the  mouth, look like grains of salt  surrounded by red ‘halo’We also discuss several other topics like math 123 notes

Treatment

Drainage of the infection and  administering antibiotics

Remove tick, administer  

doxycycline, tetracycline, or  chloramphenicol

Chickenpox – none required Shingles – bedrest, loose-fitting  bandages covering lesions

Administration of Vitamin A,  antibodies against measles  virus, and ribavirin

Prevention

Hygienic practices and infected  person contact precautions

Avoid tick infested areas and  frequent tick checks

Attenuated vaccines: Varivax  for children and Zostavax for  those 60 and older

Live, attenuated vaccine

Cardiovascular infections Lyme Disease Malaria Mononucleosis

Causative Agent

Borrelia burgdorferi

Plasmodium species

Human Herpes virus 4,

Epstein-Barr virus

Organism Characteristics

Gram- spirochete with endoflagella

Exoerythrocytic cycle

Erythrocytic cycle

Sporogenic cycle

Enveloped ds DNA virus

Reservoir

White footed mouse (zoonosis)

Monkeys (zoonosis)

Other people

Mode of Transmission

Biological Vector: ticks

Anopheles mosquitos

Saliva

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Parenteral

Blood stream

Oral

Organism’s Virulence

Factors

Lacks iron-containing enzymes, changes  outer surface proteins which confuses  immune system and endotoxin

Red blood cell replication, adhesins,  merozoites

Latency, causing lifelong infection. Lytic  replication

How Organism Affects Body

Can go dormant for a while. Most of the  signs and symptoms are caused by  immune response to bacterial presence

Extreme fever, large scale erythrocyte  lysis, renal failure, and dark urine, small  hemorrhages, tissue death

Infects epithelial cells of pharynx or  salivary glands. Virions released into the  bloodstream

Signs and Symptoms

Vast array, but generally three main  stages. Red ‘bull’s eye’ rash, neurological  (10% of cases) then severe arthritis

Fever, chills, diarrhea, headache,  pulmonary or cardiac dysfunction,  anemia, weakness, fatigue

Sore throat, fever, weakness. Swollen  lymph nodes, spleen, night sweats

Sequelae

Rarely if ever fatal

Immunity gradually develops if victim  survives acute stages

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Epidemiology

Concentrated in the Northeast and  upper Midwest

Areas with high temperature, humidity  and rainfall.

Children sometimes, but prevalent in  teens and 20’s

Diagnosis

Signs and symptoms, followed by  detection of organisms or antibodies in  the blood

Case history, and plasmodium species in  blood smears

B lymphocytes with atypical nuclei.  Antibodies to EBV (monospot test)

Treatment

Doxycycline or penicillin for first phase,  difficult to treat later

Chloroquine, mefloquine, antifever meds  and occasionally blood transfusions

Relief of symptoms. Takes two to four  weeks. Biggest danger is ruptured spleen

Prevention

Avoid ticks, use bug spray, wear long  pants, etc.

Limit contact with mosquitos,  

prophylactic drugs

Prevention almost impossible

Respiratory infections Tuberculosis Streptococcal Diseases Influenza

Causative Agent

Mycobacterium tuberculosis

Streptococcus & S. pyogenes

Orthomyxovirus

Organism Characteristics

Gram+ rod with mycolic acid

Gram+ facultatively anaerobic

ssRNA genome, enveloped

Reservoir

Humans

Humans

Birds, pigs, etc. (zoonosis)

Mode of Transmission

Respiratory droplets

Respiratory droplets

Droplet, airborne, or fomites

Portal of Entry

Inhalation

Inhalation

Inhalation

Organism’s Virulence

Factors

Mycolic acid: Slow growth, protected  from phagocytosis, intracellular growth Cord factor

M protein, hyaluronic acid capsule,  streptokinases, C5a peptidase,  Pyrogenic toxins, StreptolysinsIf you want to learn more check out genetics test study guide

Lytic replication cycle, envelope,  glycoprotein spikes (neuraminidase and  hemagglutinin)

How Organism Affects Body

Tubercles form in lungs over several  months, collagen fibers enclose  tubercle. Cavity forms and immune  system reaches stalemate. When it  breaks bacteria enter bloodstream

Infects throat, can cause strep throat  and bronchitis if normal microbiota is  depleted. SP can occasionally break  through mucous membranes

Epithelial cells are lysed, patient  susceptible to secondary bacterial infection. Cytokines from immune  response cause symptoms

Signs and Symptoms

Cough and fever progress to symptoms  corresponding to the complications  arising from wherever the bacteria are  deposited in secondary infection

Red pharynx, swollen lymph nodes,  purulent abscesses, fever, malaise,   laryngitis, bronchitis,  

glomerulonephritis, rheumatic fever

Pharyngitis, congestion, fever, dry  cough, malaise, headache, myalgia

Sequelae

Move from  blood vessels to lymphatic  system and are carried to bone marrow,  spleen, kidneys, spinal cord, or brain

Scarlet fever develops from a certain  strain of S. pyogenes when pyrogenic  toxins are released

Secondary bacterial infection

Epidemiology

Kills four people each minute, mostly is  Asia and Africa. Those with lowered  immunity at highest risk

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Changing antigens, there will always be  susceptible people. Young, elderly, and  immunocompromised are at risk

Diagnosis

Skin test, chest X-ray, sputum sample  with acid-fast cells present

Strep test, serological testing

Signs and symptoms during community  outbreak

Treatment

Common antimicrobials don’t work  because it grows so slowly. Have to be  slowly released

Sensitive to antimicrobials: penicillin

Antiviral therapy, must be started early  to be effective. Tamiflu and Relenza

Prevention

BCG attenuated vaccine. Not common  in the US because disease is not  prevalent

Keep sick children isolated and treat  immediately to avoid Rheumatic fever

Immunization with multivalent vaccine

Nervous system Bacterial meningitis Viral meningitis

Causative Agent

Over 50 species (some opportunistic)

Enterovirus

Organism Characteristics

N. meningitides – Gram- diplococcus

S. pneumoniae – Gram+ coccus

Small, non-enveloped, RNA

Reservoir

Humans

Humans

Mode of Transmission

Respiratory droplets

Fecal contamination of food and sometimes  respiratory secretions

Portal of Entry

To meninges via bloodstream

Infect GI tract or lungs, then bloodstream

Organism’s Virulence

Factors

NM: Capsule, fimbriae, and lipooligosaccharide  SP: IgA protease, capsule, phosphorylcholine

Viruses can cross blood brain barrier more easily

How Organism Affects Body

Inflames spinal meninges, puts pressure on  surrounding nerves and muscles, neck grows stiff  and some sensory and motor control affected

Spreads from blood to lymph system, then  crosses blood-brain barrier. Kills cells in meninges

Signs and Symptoms

Encephalitis, Increase in white blood cells in  cerebrospinal fluid, petechiae, sudden fever, and  meningeal inflammation

More mild than bacterial meningitis but  headache is worse, fever, stiff neck, drowsiness,  confusion, nausea

Sequelae

100% of untreated cases lead to death

Death is rare

Epidemiology

NM – children and young adults

SP – age extremes, babies and old people

Very common and very contagious. Neonates are  at highest risk of morbidity and mortality

Diagnosis

Culturing bacteria from cerebrospinal fluid tap Serological tests for antibody presence

Signs of meningitis with no bacteria in CSF. Blood  tests also available

Treatment

Antimicrobial drugs

Bed rest, fluids, medication for symptoms

Prevention

NM: MPSV4 (Menomune)  

MCV4 (Menveo, Menactra)

SP: PPV (Pneumovax) PCV (Prevnar 13)

Hard to prevent, so just wash your hands

STI/STD Gonorrhea Chlamydia Genital Warts

Causative Agent

Neisseria gonorrhoeae

Chlamydia trachomatis

Papillomaviridae

Organism Characteristics

Gram – diplococci

Susceptible to drying

Gram-, intracellular obligate, nonmotile

Non-enveloped, DNA viruses

Reservoir

Humans

Humans

Humans

Mode of Transmission

Sexually transmitted (direct contact)

Sexually transmitted (direct contact)

Direct contact and fomites

Portal of Entry

Urethra, vagina, and anus

Mucous membranes

Urethra, vagina, and anus

Organism’s Virulence

Factors

Fimbriae, capsule, Lipooligosaccharide,  IgA Protease, multiply in neutrophils

Most common sexually transmitted  BACTERIUM in the US

Extremely contagious. Most common  sexually transmitted DISEASE in the US

How Organism Affects Body

Adhere to mucous membranes of  genital, urinary, and digestive tracts.  Attach to cervix (not vagina) and to  sperm via fimbriae. Infection during  childbirth can lead to blindness

Elementary body attaches to receptor to  trigger endocytosis, then reticulate body  replicated inside vesicle. Convert back  into EB’s, lyse the cell and infect other  neighboring cells.

Low risk: doesn’t cause cancer. Causes  genital warts

High risk: integrate into human  chromosomes. Linked to many cancers,  especially cervical

Signs and Symptoms

Men: urethritis, discharge from penis,  scarring of prostate

Women: 50-80% asymptomatic, burning  urination, yellow or bloody discharge

Most people do not experience signs  and symptoms. Men may experience  discharge or burning urination.

Development of warts within 3 to 4  months after infection, however many  HPV infections never exhibit this sign

Sequelae

Men: may result in infertility

Women: could lead to infertility or pelvic  inflammatory disease

Can lead to sterility, pelvic inflammatory  disease, and ectopic pregnancy. Makes a  point of entry for other pathogens

Development of cervical, anal, vaginal,  penile, and oral cancers

Epidemiology

Adolescents with multiple sexual  partners in the southeast. More  common in males

Most prevalent in women less than 20  years old because the cervix isn’t fully  matured yet

6.2 million new cases every year in the  United States. More than half of sexually  active adults are infected

Diagnosis

Gram- diplococci in penal discharge.  Asymptomatic people can be diagnosed  with commercially available probes

Chlamydial DNA found in cells at site of  infection

Abnormal PAP smear results, DNA  probes, other observation

Treatment

Treatment with two antibiotics at the  same time

Doxycycline or Erythromycin for 21 days

Warts removed (however viruses often  remain in surrounding tissue)

Prevention

Reinfection is common. Surface antigens  are variable. Condom use is effective

Condoms provide some protection, but  not always effective as they can cause  abrasions

Gardasil

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