Flashcards: final study guide LETS GOOOOOO

-On skin and mucous membrane

Non-motile, non-spore forming, Gram(+) cocci in clusters

•Resistant to temperature, osmotic pressure (high salt concentration), drying

-catalase (+)

commensals (many bacteria)

•S. aureus

•S. Epidermidis, S.capitis, S.hominis

•S. saprophyticus

S. Aureus- most resistant 

Withstand salt, Ph, temp, drying, disinfectants

Coagulase :clots plasma, can prevent phagocytosis

•Opportunistic infection

invade the host

•Hyaluronidase  ->  Destroys host tissues

•Hemolysins  ->  Lyse RBCs

•Leukocidins  ->  Destroys WBCs

Abscess- pus 

Folliculitis- inflammation of hair follicles

-systemic: Endocarditis (heart)

Hidradenitis- inflammation of gland

Furuncle- boil from hair follicle

- systemic Osteomyelitis (bones)

Carbuncle (large)-> Pneumonia (lungs)

healthcare associated infections (endocarditis, bacteremia, UTI’s)

UTI’s in sexually active women

Folliculitis (hair follicle)->  Endocarditis (heart)

Furuncle (boil) -> Osteomyelitis (bones)

Carbuncle (large)-> Pneumonia (lungs)

Enterotoxin

•Food intoxication: Enterotoxin is heat resistant, vomit

•Staphylococcal scalded skin syndrome toxin causes SSSS in umbilical/ eye babies and bullious impetigo in all ages

•Toxic shock syndrome: superantergen TSS toxin

fever, shock, low blood pressure, can be fatal

•Toxin is released in high levels when magnesium is not present(low flow)

drainage

resistant to penicillin

–cillins, cephalosporins, sulfa drugs, tetracycline

•Vancomycin, quinupristin “drug of last resort”

•MRSA: Methicillin resistant Staphylococcus aureus- use vancomycin

•

•VRSA: Vancomycin resistant Staphylococcus aureus •quinupristin/dalfopristin

Catalase test: Staphylococcus catalase +, strep catalase-

Coagulase test: Staphylococcus aureus coagulase + other Staphylococcus coagulase -

Serological tests:  Antibody based tests can identify S. aureus quickly

•Non-motile, non-spore forming

Gram (+) cocci in long chains.

Facultative anaerobes,

do not survive well outside the host

Lancefield groups: type of carbohydrates on cell wall

A- S. pyogenes

B- S. agalactiae

D- Enterococcus facecalis,

H S. sanguinis

S mutans and S. pneumonia none

Group A (GAS) Streptococcus pyogenes

pyoderma (impetigo)- skin infection

•Streptococcal pharyngitis (Strep throat)

scarlet fever- if erythrogenic toxin=

necrotizing fasciitis (“flesh-eating disease”)- below skin

S. pyogenes pneumonia

Long term complications

•Rheumatic fever: joints and heart.  May damaged heart valves

•Glomerulonephritis:  Kidney damage.

Group A

Gram+ cocci, non motile non spore forming.

Beta hemolysis

sensitive to bacitracin

C-carbohydrate on surface to prevent lysozyme

strep throat, scarlet fever, rheumatic fever, glomerulonephritis

•C-carbohydrate on wall,: Protects against lysozyme

•M-protein: Fimbriae. Resists phagocytosis and adhere to host cells

•C5a protease: Inhibits one of the proteins in the complement cascade

•Hemolysins:  Streptolysin S (SLS), Streptolysin O (SLO) Attacks kidney, heart, muscle

•Some strains of S. pyogenes carry a prophage for erythrogenic toxin(pyrogenic) that produce fever and red rash

•Streptococcus agalactiae

•β-hemolytic

found in vagina

•Causes wound infections in elderly and diabetic

•Meningitis in newborns when women has •S. agalactiae while birth

•Penicillin is effective treatment

pneumococcus

pairs and short chains, α-hemolytic,

no Lancefield group

thick capsule (phagocytosis difficult)

•Infection: otitis media (middle ear infection) in children

meningitis- all age

pneumonia in older adult/ immune compromised

•Vaccines: Prevnar 13 (13-valent), Pneumovax (23-valent)

•Penicillin or cephtriaxone are effective treatments

Neisseria,

Branhamella,

Moraxella

Non-motile, non-spore forming, bean shaped diplococci.  Fastidious.

•gram - , fimbriae, catalase

•Two main pathogens

•Neisseria gonorrhoeae

•Neisseria meningitides

Gonococcus- spread thru sex, birth,

•Pili, Capsules, Protease which inhibits IgA, Lipopolysaccharide  

presence of cells within neutrophils = infection

Painful urination

female: may be asymptomic

salpingitis- type of pelvic inflammatory disease (PID) ectopic pregnancy (baby outside uterus)

•Combined drug therapy with ceftriaxone and azithromycin (resistance to penicillin in PPNG strains)

Birth: tetracycline or erythromycin ointment  is always applied to the eyes

Neisseria meningitidis-

gram - cocci, diplococci, positive oxidase, ferment maltose not sucrose/lactose

capsule and fimbriae, endotoxin

Meningitis

cerebrospinal meningitis- inflammation of brain/spinal cord

•Fever, stiff neck, photophobia, confusion

Meningococcemia

meningococcal septicemia (bloodstream infection)

•Fever/chills, cold hands and feet, vomiting, dark purple rash (petechiae)

spread thru respiratory secretions

• vaccine

Menactra, Menveo

Bexsero, Trumenba(serotype B for child)

•Treatment: broad spectrum antibiotics ceftriaxone

•Close contacts: prescribed prophylactic antibiotics (rifampin or ceftriaxone)

Bacillus 

Clostridum

Endospore formers? 

Oblige anaerobe vs aerobic/faculative anaerobe

Regular shape/ staining properties

Acid fast, filamentous branching cell

Bacillus anthracis

Clostridium tetani

Clostridium perfringens

Clostridium botulinum 

Clostridioides difficile

Listeria monocytogenes

Corynebacterium diphtheria

Mycobacterium tuberculosis

Mycobacterium leprae

People who work with animal

• in soil/GI tract of animals

•Obligate anaerobe

•Produces tetanospasmin (toxin)

•Causes tetanic paralysis(muscle lock)

•prevent Vaccine (tetanus toxoid)

•Treatment

•Human tetanus immune globulin (HTIG)

•antibiotics: metronidazole or penicillin

•Mechanical ventilation/muscle relaxants

•Gas gangrene (Myonecrosis)infection of soft tissue and food poisonings

•Obligate anaerobe

•Mixed infections

•Treatment

•Cleansing/debridement of wounds

•Clindamycin, antibiotics

•Hyperbaric oxygen treatment

•Spores on soil, water, animal intestine

droopy eyelid, hard to speak

•Descending flaccid paralysis(motor), death from paralysis of respiratory muscles 

•Botulinum toxin:

•Prevent release of acetylcholine ( botox)

•food intoxication, Infant botulism (floppy baby syndrome), Wound

Prevention: boiled for 10 minutes

no honey for baby

don't inject

Treatment

antitoxin (anti-botulinum antibodies) mechanical ventilation

C-Diff

normally small amount in intestine

diarrhea, inflamed colon,

ELISA to detect toxins in fecal samples

long term broad antibiotic causes superinfection

Treatment

•Withdrawal of antibiotics

vancomycin or metronidazole

•Fecal microbiota transplantation (eat poop)

irregular- stain unevenly

Corynebacterium, mycobacterium, nocardia

Regular

Listeria & eysipelothrix

•Listeriosis

•Gram-positive, regular, rods

grows in cold, psychrotroph

•found in dairy, poultry, and processed meat

•immunodeficient patient-affect brain, meningitis

•Pregnant woman (miscarriage, birth defects)

•Prevention/Treatment

•Pasteurization, adequate cooking

•Antibiotic, ampicillin/gentamicin and trimethoprim sulfamethoxazole

Corynebacterium diphtheria

0.01 case per million population extremely rare in US thanks to vaccination DTap (no cases since 2014)

•16,000 cases reported worldwide

•Gram-positive, irregular rods

• production of diphtherotoxin, which affects heart and nerves

•Antibiotics to stop infection

•Antitoxin to reverse effects of toxemia

Mycobacterium

•Low infectious dose

resistant to drying and germicides

•Very slow growing 

•Cord factor (allows cells to form long aggregates)

•Most species are saprobes, but several pathogens exist

•Mycobacterium tuberculosis

•Mycobacterium leprae

Mycobacterium leprae (leprosy)

humans and armadillos

predisposing factor: defective T cell, poor health, long term contact with it

years of incubation for disease

•Single lesion paucibacillary (SLPB)-spots

if untreated:

•Paucibacillary (PB) hypopigmented patches, loss sensation

•Multibacillary (MB): • necrosis and disfigurement (sport and death of cell)

•Treatment: long-term antibiotic therapy

Mycobacterium tuberculosis

Cord factor is responsible for long strands of cell upon examination and is correlated with increased virulence

•Primary TB: tubercles in lung (red areas). mild fever

•Secondary TB: Reactivated primary disease: coughing, fever, bloody sputum, weight loss. 60% mortality if untreated

•Extrapulmonary TB: Spread of cells to other organs, lymph nodes, kidneys, brain. Usually fatal

long-term antibiotic therapy sane as TB

•Multidrug therapy for 6-9 months

•First line drugs

•Isoniazid

•Rifampin

•Ethambutol

•Pyrazinamide

•Second line drug (Pretomanid) used for MDR-TB and XDR-TB

•Multidrug therapy for 6-9 months

•First line drugs

•Isoniazid

•Rifampin

•Ethambutol

•Pyrazinamide

•Second line drug (Pretomanid) used for MDR-TB and XDR-TB

Lipopolysaccharide(LPS) which act as endotoxin to produce systemic effect

gram - rod aerobe

on soil, sea water, fresh water

highly versatile

degrade natural substance, food spoil

in homes and hospital

•Obligate aerobe

•Cause of Pertussis whooping cough,

endotoxin destroy cell

•Catarrhal stage: Cold-like

•Paroxysmal stage: Severe coughing “whoops”

•

•Adults: mild symptoms

•Infants: highest risk of death

•Acellular vaccine (aP in dTaP)

•Five doses plus a booster at 11-12, not completely effective

•Treatment-Azithromycin or clarithromycin

•Obligate aerobe

•Blue/green pigment

slime layer, enotoxin, endotoxic shock

•soil/water and intestine of health people

hot tub, soap, sponge,

opportunistic: Burn/cystic fibrosis patients

•cause Endocarditis, pneumonia, meningitis

•Healthy patients: rash, UTI, external ear infection

•Susceptibility testing required

•Extensive drug resistance

cephalosporin, aminoglycoside, polymixin

Legionella pneumophilia

•Obligate aerobe

•Cause of Legionnaires disease

•Fever, cough, may progress to pneumonia

•Opportunistic

•Air conditioning, hot tubs, showerheads, vegetable sprayers + natural sources

•Legionella survive within various protists, and phagocytes within humans

•Prevention: chlorination and elimination of standing water

•Treated: Levofloxaxin broad spectrum antibiotics

•Pontiac fever: Mild, related disease, self limiting

H- flagellar antigen

K- capsule and fimbrial antigen

O- somatic or cell wall antigen

•Reservoir in intestines of cattle

•Traveler's diarrhea, Infantile diarrhea can be deadly

•STEC: Shiga toxin producing E. coli

•O157:H7: cause hemorrhagic colitis

•Hemolytic Uremic Syndrome (HUS),Kidney damage

•50%-80% of Urinary Tract Infections (UTIs)

indicator of fecal contamination of food/water\

•Control: clean food, pasteurization

hydration and rest

Bismuth salicylate (pepto bismol)

Enterohemorrhagic(EHEC) or STEC- damage to kidney

Enterotoxigenic (ETEC)- small intestine

Enteroinvasive(EIEC)- large intestine

Enteropathogenic(EPEC)- infantile diarrhea

Enteroaggregative(EAEC)- intestinal mucosa

Dissusely adgerent(DAEC)- pediatric diarrhea

Salmonella enterica Typani cause typhoid fever

Salmonella Paratyphi- paratyphoid disease

Human host

Antibiotic treatment- ciprofloxacin or ceftriaxone

Salmonella bongori- cold blooded animal like lizards

•Nontyphoidal salmonelloses

other Salmonella serotypes

, causing diarrhea.  Lasts 2-5 days

•Normal microbiota of cattle, poultry, rodents, reptiles

•Uncooked/unpasteurized milk, meat, eggs present risk

•Typhoid fever, diarrhea

Washing food, and hands

•Shigellosis

invasion of large intestine from five Fs

•Feces, food, fingers, flies, fomites

•Shiga toxin lead to bleeding and heavy mucus

•Bloody, mucus-filled diarrhea

•Damages nerve cells, intestines, kidneys

Treatment: ciprofloxacin or sulfatrimethoprim

•Bubonic plague: enlarged lumph bubos (swollen lymph nodes)

•Black death: darkening of skin

•Pneumonic plague: Localized to lungs

•Found and Spread through bite of infected fleas, handling infected animals

•Prevention: quarantine/kill animal hosts

•Treatment with broad antibiotics: streptomycin, gentamicin, doxycycline and ciprofloxacin

Treponema 

Leptospira 

Borrelia

Treponema pallidum

•Sexually Transmitted Disease (STD or STI)

•Fastidious.  Doesn’t survive long outside the body

•Primary syphilis: Hard chancre at point of contact (genitals, mouth)

•Secondary syphilis: Spread of bacterium. (don’t treat primary becomes secondary) Fever headache, sore throat “Nickel and Dime” rash on the palms and soles

•Tertiary syphilis: Occurs after long (20 year) latent period. Damage to multiple organs untreated

•Gummas: Tumors

•Neurosyphilis: Blindness, convulsions, mental deterioration

•Argyll-Robertson pupil (pupil not round)

Penicillin G for all stages

Leptospira interrogans

•Zoonosis, found in many animals

•Bacteria are shed in the urine of infected animals(cuts, usually in streams)

•Disease is concentrated in tropics, most U.S. cases found in Hawaii

•Flu-like disease, progresses to include hallucinations

•Serological detection

•Early treatment with doxycycline is effective 

•Human infection is transmitted by ticks or lice

•Two major species

•Borrelia hermsii: Relapsing fever (antigen mutation ensure relapse)

•Borrelia burgdorferi: Lyme disease

•Relapsing fever occurs because the spirochete changes its surface antigens, so antibodies only protect for a short time

•Treatment is doxycycline

•Prevention relies on avoiding ticks and lice

•Borrelia hermsii: Relapsing fever (antigen mutation ensure relapse)

•Borrelia burgdorferi: Lyme disease

•Borrelia burgdorferi:

•Lyme disease, spread by ticks, endemic to NE U.S.

•70% of cases display bullseye rash

•Without treatment, disease progresses to neurologic, cardiac and arthritic symptoms

•Detection relies on serological testing (ELISA)

•Early treatment with doxycycline,

prevention: avoid ticks and outdoors

Vibrio cholerae

dirty water

•death via secretory diarrhea due to cholera toxin 

•Treatment: replacement of electrolytes (Gatorade) and antibiotics

•Prevention: water purification and proper sewage disposal

•Vaccine: limited protection for ~2 years

•Rare in the U.S.

Vibrio parahaemolyticus

•Salt tolerant microbes, severe gastroenteritis

•consumption of squid, mackerel, tuna, oysters etc.

•Prevention: proper refrigeration/cooking of seafood

Vibrio vulnificus

• more severe

• lethal in individuals with diabetes/liver disease

•enter wounds and cause disease

•Prevention : cook/storage of seafood. no brackish water with cuts

Salty water

curved, spiral bacilli in S shape, gull winged pair. spinning motility

•Cause Campylobacter gastroenteritis(stomach ache)

•Common resident of birds and mammals (raw chicken)

•CJT:  Enterotoxin that stimulates secretory diarrhea

•75 deaths, mostly compromised patients

•Treatment :replacement of electrolytes

•Cause of stomach and duodenal ulcers

•Favors a low pH environment

•Treatment centers on antibiotic therapy plus acid inhibitors

•Tiny parasitic bacteria

•Part of life cycle takes place in arthropod vectors (lice, fleas, ticks)

•Major diseases are typhus and spotted fever

•Epidemic typhus

•Carried by lice (associated with overcrowded living conditions)

•Flulike, rash, mortality up to 60% in older patients

•Treatment: antibiotics doxycycline or chloramphenicol , along with anti- louse soap/shampoo

insecticides of living spaces

•Endemic typhus, worse than prowazekii

•Carried by fleas

•workers in rat infested sites

•Flu-like, rash, milder symptoms than R. prowazekii

•Treatment: antibiotics doxycycline or chloramphenicol

•Cause of Rocky Mountain Spotted Fever

• Eastern US Transmitted by ticks thru dog then to human 

•Flulike + red spotted rash, cardiovascular and CNS involvement

•Detected via ELISA or PCR

•Treatment: doxycycline

avoidance of tick bites

•Outer protein coat, inner nucleic acid

•RNA or DNA, not both

•Some viruses possess envelope and spikes

•Envelope derived from host cell membrane

•Spikes aid in attaching to host cells

•Host range/tissue tropism

RNA or DNA, not both need a host for metabolism

Symptoms! (virus attack specific host range, lung)

•Serological detection of envelope, viral spikes, or production of antibodies against a virus

•Polymerase chain reaction of viral DNA/RNA 

Poxvirus

fever, malaise, prostration and rash

variola major: toxemia shock and intravascular coagulation

HSV-1

•Herpes keratitis (ocular herpes): spreads to the eye via fingers or the ophthalmic branch of the trigeminal nerve

Herpetic whitlows: Health care workers

HSV-2 Genital lesions

•Neonatal herpes: during birth

•Split between HSV-1 and HSV-2

can be deadly for baby

•Acyclovir limits viral shedding during third trimester

C-section

Chickenpox when reactivated (x-rays, drugs, surgery…) shingles

•Cause of chickenpox in children (rash spread across face and trunk)

•Shingles appears as a single limited rash (dermatome)

•Post-shingles neuralgia can cause months-long pain

•Patients with shingles can infect others with chickenpox

•Both diseases are diagnosed based on symptoms

•Vaccine protects against chickenpox

•Vaccine after age 50 protects against shingles

•Acyclovir may lessen symptoms

Poxviruses 

Herpesviruses

Hepadnaviruses

Adenoviruses

Polyomaviruses

Papillomaviruses

Parvoviruses

Poxvirus

Epstein-Barr Virus (a herpes virus)

•Infectious mononucleosis

•Found in lymphoid tissue and salivary glands

•“kissing disease”

•Sore throat, swollen tonsils, fever, malaise

• Burkitts lymphoma: B-cell cancer that swells the cheek

•Immunocompromised patients

•Diagnosed via abnormal white blood cells, PCR

•Treatment: relief of symptoms

Ganciclovir may be used to help airway

Hepatitis B (a hepadnavirus) DNA virus

•bilirubin causes jaundice

•Fever, rash

•Spread via blood, sexual contact, needles

•Chronically carried (long term)

•Risk of cirrhosis liver cancer

•Detection via serological testing

• vaccine for under 18

•Treatment for severe infection: interferon and Hepatitis B immune globulin (HBIG)

Nonenveloped and single stranded

•Cause of warts, genital wart

•Spread via contact with warts or, less often, fomites

strains HPV 16 and 18

•70% of metastatic tumors (cervix and penis)

•Gardasil 9 Vaccine protects against the nine strains most strongly linked to cancer

•Recommended for children 11-18 (prior to sexual activity) 

Orthomyxoviruses -influenze

Bunyaviruses- hantavirus pulmonary syndrome

Arenavirus- Lassa fever

•Antigenic drift

•Nonsegmented genomes change slowly over time via mutation

•Immunological memory offers protection

•Antigenic shift

•Segmented genomes may join within a single cell creating a unique virus

•Leads to rapid change in virus

•No immunological memory

Orthomyxovirus: Influenza

•Two types of surface spikes

•Hemagglutinin: Allow virus to bind to respiratory receptors (18 types)

•Neuraminidase: Breaks down mucus, assists budding of new viruses from host cell.

•Flu viruses named for their combination of H and N spikes 

50,000 deaths/year. Mostly old, young

•Injectable vaccine: Inactivated virus

•Inhaled vaccine: Live virus

•High dose vaccines are available for older patients

•Treatment:

•Relenza, Tamiflu, Rapivab : Block viral budding and release

•Xofluva: Blocks viral RNA synthesis

hantavirus

•Hantavirus pulmonary syndrome

•Severe pulmonary (lung) disease

•Carried by deer mice feces (Yosemite)

•Southwest U.S.

parainfluenza and

•Mumps: Swollen parotid glands, flulike symptoms

•Spread respiratory secretions

•Diagnosed: symptoms/serological testing

•Prevention through vaccination (MMR)

•Few thousand cases per year in small outbreaks

Morbillivirus: Measles (Rubeola) 

•Severe, flulike symptoms

•Extremely contagious

•Identified by skin rash, Koplik's spots in mouth

•Complications

•Subacute sclerosing panencephalitis (SSPE): Occurs 7-10 years later, ends in coma and death

•Deafness, neurological deficits

•Pneumonia

•Immune amnesia: Memory T and B cell for diseases other than measles are lost.  Leaves patients vulnerable 

•Prevention relies on vaccination (MMR)

•Treatment is based on alleviating symptoms 

Paramyxoviruses- Measles, mumps

Rhabdoviruses- rabies

Filoviruses- Ebola fever

Corona virus- SARS, MERS

Togavirus- Rubella

Flavivruses- Dengue fever, Zika virus

Rhabdovirus: Rabies lyssavirus 

•Slowly progressing, neurologic, zoonotic disease

•1-3 human cases/year, 40,000 people/year receive post-exposure prophylaxis (U.S.)

•Neurological symptoms

•Furious phase: seizure, twitching, hydrophobia

•Dumb phase: paralyzed, disoriented, coma, death

•Untreated disease is 100% fatal

• bite of unprovoked mammal

•Treatment: passive immunization with human rabies immune globulin (HRIG) on day 1 and vaccination on days 1, 3, 7, and 14. 

•Negri bodies in brain tissue may be seen upon autopsy

•Wild animals may be vaccinated to reduce vectors

Ebola and Marburg Virus 

Contact with infected animal/fluid of infected person

•Ebola treatment with monoclonal antibodies (Inmazeb) approved October 2020

supportive care

•Marburg virus has no treatment or preventative beyond supportive care

•2002 SARS (severe acute respiratory syndrome)

•2012 MERS (Middle East Respiratory Syndrome, MERS-CoV)

•2019 Novel coronavirus (SARS-CoV-2)

•SARS-CoV-2 spreads mostly via respiratory droplets

•Droplets don’t stay airborne long

SARS-CoV-2 binds to angiotensin-converting enzyme 2 (ACE2), on cell membrane of lungs, vascular epithelium, kidneys, other tissues

•SARS-CoV-2 can induce hyper-immune response in some people (severe disease)

•Cytokine release syndrome: Systemic inflammation driven by T cells (mostly IL-6)

•Organ failure: kidney, heart, liver

•Inflammation of the vasculature allows blood and fluid to fill the lungs leading to acute respiratory distress syndrome (ARDS)

•~70% of deaths due to ARDS

•~30% of deaths due to multi-organ failure

Treatment

•Maintenance of oxygen levels

•Treatment of bacterial and fungal infections

•Dexamethasone: Steroid. Reduces immune response

•Remdesivir: Inhibits viral RNA polymerase

•Paxlovid: Inhibits protease needed for replication

•Molnupiravir: Cause multiple mutations in the viral RNA

•Paxlovid and Molnupiravir can both be taken after symptoms occur and can shorten course of disease.

•Monoclonal antibody therapy

•Bamlanivimab: Binds to viral spikes, prevents entry of virus into cells.

Prevention

•Moderna and Pfizer vaccines are mRNAs that invade muscle and epithelial cells (like a virus) and produces viral spike proteins

•Proteins elicit an immune response

•Nucleic acid amplification tests (NAATS)

•PCR (polymerase chain reaction), others

•Used to intensify coronavirus RNA

•Do you have the virus in your body?

•Nasal swab

•Accurate even without symptoms

•

•Serological testing

•Do you have antibodies against the virus?

•IgM: new infection

•IgG: old infection

•Most accurate after symptoms have begun  

Togavirus

Rubella (German measles)

•spread through respiratory and college dorm

•Teratogenic when pregnant women are infected (congenital rubella syndrome)

•Eliminated from U.S. in 2004, still prevalent worldwide

•Prevented through vaccination (MMR)

Flavivirus

• blood contact, needles (not generally sexual)

• increased risk of liver cancer

•Diagnosed by detecting antibodies to the virus

•Treatment: Harvoni, a combination of two drugs, taken for 12 weeks

•93%-99% cure rate

(Arthropod born)

•Fever, rash, flu-like symptoms, hemorrhagic fever(bleed from eyes), maybe meningitis

•West Nile Virus, Colorado tick fever, Yellow fever, Various encephalitides

•Sentinel animals track spread

•Aedes aegypti mosquito-borne viruses

•Chikungunya

•Dengue: breakbone fever

•Zika: Birth defects: microcephaly

•Sexual transmission

•Control

•Yellow fever: Vaccine

mosquito control

•Backward (retro) flow of genetic info RNA ->DNA

•Reverse transcriptase produce DNA from RNA genome

•Viral DNA integrates into host cell genome

•Three retroviruses infect humans

•Human T cell Leukemia virus I and II (HTLV-1, HTLV-2)

•Human Immunodeficiency Virus (HIV)

•HIV has two envelope proteins (spikes) that allow binding to CD4 host cells

•GP-120

•GP-41

cause of Acquired Immune Deficiency Syndrome (AIDS)

•HIV is spread through blood and sexual contact, where it enters macrophages and dendritic cells

•HIV entry occurs when GP-120/GP-41 bind to three receptors on CD4 cells

•CD4•CCR5•CXCR4

CD4, T4, monocyte, dendritic, macrophage

•Nonprogressor: People exposed to HIV without infection, Lack CCR5 or CXCR4 receptors

•Initial lytic infection marked by high viral load

•Viral load decreases as anti-HIV antibodies are produced

•Virus exists in white blood cells for 2-15 years without symptoms

•T cells eventually plummet, immune system collapses, AIDS begins

Infection with HIV, and

At least one of

•CD4 count fewer than 200 cells/microliter of blood

•CD4 cells are less than 14% of total lymphocytes

•Experience an AIDS-Defining Illness (all are opportunistic diseases) 

•ART (antiretroviral therapy)

Binding inhibitor block receptors on CD4

fusion inhibitor- prevent fusion with CD4 membrane

Nucleoside reverse transcriptase inhibitors (NRTI)- stop RNA to DNA

Non nucleoside reverse transcriptase inhbitor (NNRTI)- prevent enzyme from functioning

Integrase inhibitor

Protease inhibitor- prevent activation of assembled virus

•interrupting viral replication cycle with multiple drug

(Pre-exposure prophylaxis)

•Two drugs (non-nucleoside reverse transcriptase inhibitor + nucleoside reverse transcriptase inhibitor)

•Reduces risk of HIV infection 99%

•Descovy, Truvada

HIV infection is diagnosed by looking for antibodies to HIV

•ELISA, agglutination, or similar test

•Testing is a two-step process

•1^st test: High sensitivity, but more false positives (ELISA etc.)

•2^nd test (confirmatory): High specificity (Western blot)

•Testing window: Virus is present for a few weeks, then disappears

•Antibodies may not be produced until months after infection

•Negative tests should be repeated 3-6 months later

•Testing for the virus itself may be done for blood or organ donation, or to monitor HIV load in people being treated

•HIV infection is diagnosed by looking for antibodies to HIV

•ELISA, agglutination, or similar test

•Testing is a two-step process

•1^st test: High sensitivity, but more false positives (ELISA etc.)

•2^nd test (confirmatory): High specificity (Western blot)

•Testing window: Virus is present for a few weeks, then disappears

•Antibodies may not be produced until months after infection

•Negative tests should be repeated 3-6 months later

•Testing for the virus itself may be done for blood or organ donation, or to monitor HIV load in people being treated

•Inactivated vaccine (Salk vaccine): Used in low-risk areas (including U.S.)  

•Live vaccine (Sabin vaccine) Used in high-risks areas of world

•Eliminated from Americas 1991

Hepatitis A  (A picornavirus)

•Dissimilar to hep B and hep C

•oral fecal, inadequate hygiene

•Flulike symptoms, complete recovery

•Multiple vaccines exist (HAVRIX, VAQTA)

•TWINRIX :protection against Hep A and Hep B

Caliciviruses

•Norwalk virus/Norovirus

•Vomiting, diarrhea, cramps

•Spread via the oral-fecal route

•Low infectious dose

•crowded spaces

•Double stranded RNA virus (dsRNA)

•Spread via oral-fecal route

•Infection in U.S. is common, but mild

•Fluid replacement

•Prevention via vaccine

•RotaTeq, Rotarix

Aerobes, faculative anaerobe, obligate anaerobe(no true pathogen)