Chapter 13: Microbe-Human Interactions *****TEST 3

normal resident microbiota

microbes that engage in mutual or commensal associations with humans belong to this

infection

a condition in which pathogenic microbes penetrate host defenses, enter tissues, and multiply

pathogen

microbe acting as infectious agent

infectious disease

an infection that causes damage or disruption to tissues and organs

transients

microbes that occupy the body for only short periods

residents

microbes that become established

human microbiota

skin and its contiguous mucous membranes, upper respiratory tract (oral cavity, pharynx, nasal mucosa), go tract (mouth, colon, rectum, anus), outer opening of urethra, external genitalia, vagina, external ear and canal, external eye (lids, lash follicles)

origins of resident microbiota

generally stable, but fluctuates with general health, age, diet, hygiene, hormones, drug therapy

microbial antagonism

microbiota benefits host by preventing overgrowth of harmful microbes

endogenous infections

occur when normal flora is introduced to a site that was previously sterile

initial colonization of fetus and newborn

uterus normally sterile until just before birth, subsequent handling and feeding of newborn continue to introduce what will be normal flora, nature of the microbiota initially colonizing large intestine is influenced by whether the baby receives breast milk or formula

skin microbiota: 2 cutaneous populations

transients: cling to the surface but do not grow there, influenced by hygiene

residents: stable, predictable, less influenced by hygiene, primarily bacteria, yeasts

microbial residents of gi tract

long hollow tube, bounded by mucous membranes, tube is exposed to environment, variations in flora distribution due to shifting conditions, oral cavity, large intestine, rectum harbor appreciable flora

microbiota of the mouth

most diverse and unique flora of the body, aerobic, teeth eruption establishes anaerobic habitat in the gingival crevice favoring colonization by anaerobic bacteria

adaptive niches in microhabitats

cheek epithelium, gingiva, tongue, floor of the mouth, tooth enamel

microbiota of large intestine

anaerobic bacteria, many species provide useful byproducts to host, fermentation of waste materials in the feces generates vitamins and acids

inhabitants of the respiratory tract

oral streptococci, first organisms to colonize, nasal entrance, nasal vestibule, anterior nasopharynx (staphylococcus aureus), mucous membranes of nasopharynx (neisseria species), tonsils and lower pharynx

microbiota of the genitourinary tract

sites that harbor microflora (females: vagina and outer opening of urethra, males: anterior urethra) iInternal reproductive organs kept sterile through physical barriers, kidney, ureter, bladder, upper urethra kept sterile by urine flow and bladder emptying, changes in physiology influence composition of normal flora

probiotics

introducing known microbes back into the body

primary pathogens

capable of causing disease in healthy persons with normal immune defenses, Influenza virus, plague bacillus, malarial protozoan

opportunistic pathogens

cause disease when the host's defenses are compromised or when they grow in part of the body that is not natural to them, Pseudomonas sp. and Candida albicans

virulence factor

characteristic or structure that contributes to the ability of a microbe to cause disease

portal of entry

characteristic route a microbe follows to enter the tissues of the body

exogenous agents

agents originate from sources outside the body

endogenous agents

already exist on or in the body (normal flora)

portals of entry examples

skin: nicks, abrasions, punctures, incisions

gi tract: food, drink, other ingested materials

respiratory tract: oral/nasal cavities

urogenital tract: sexual, displaced organisms

transplacental

TORCH

pathogens that infect during pregnancy

T: toxoplasmosis, O: other diseases (syphilis, varicella-zoster virus, parvovirus B19, HIV)

R: rubella, C: cytomegalovirusand

H: herpes simplex virus

hep b ca

Hepatitis B virus

hep b s&s

s&s may not be apparent until years after initial infection, general ill health, jaundice, abdominal pain, fatigue, nausea, vomiting, appetite loss, fever, dark urine, jt pain

hep b long-term effects

chronic infection occurs in: 90% of infants infected at birth, can develop cirrhosis liver failure

hep b transmission

blood from an infected person• sex with an infected person without using a condom, sharing drugs, needles, needle sticks or sharps exposures, birth, HBV can survive outside the body at least 7 days and still be capable of causing infection

hep b epidemiology

new infections decling, 20-49 yrs, asian/pacific islanders

hep b pathogenesis

bloodstream carries to liver; HBsAg allows virus to attach, liver damage likely from cell-mediated immune response

hep b prevention

vaccine, latex condoms, correctly and everytime, infants born to HBV-infected mothers- vaccine within 12 hrs after birth.• no drugs with needles, do not share personal items that might have blood on them (razors, toothbrushes)

hep b tx

5 different drugs

infectious dose

minimum number of microbes required for infection to proceed, microbes with small IDs have greater virulence

adhesion

microbes gain a stable foothold at the portal of entry; dependent on binding between specific molecules on host and pathogen: fimbriae, pili, flagella, capsules

exoenzymes

bacteria produce extracellular enzymes that dissolve barriers and penetrate through or between cells to invade underlying tissues

endotoxins

secreted by bacteria damage target cells, which die and begin to slough off

blocked phagocytic response

encapsulated bacteria can escape phagocytosis and continue to grow and cause further infections

toxins

specific chemical product of microbes, plants, some animals that has poisonous effects on other organisms

toxinoses

adverse effects of toxins

toxemias

when the toxin is spread by the blood from the site of infection

intoxications

caused by ingestion of toxins

endotoxins

bacterial toxin, not secreted, but released after the host cell is damaged, composed of part of the outer membrane of gram-negative cell walls - lipopolysaccharide

exotoxins

secreted by a living bacterial cell into the infected tissue, strong specificity for a target cell, disrupting its membrane, hemolysins, disrupt membrane of red blood cells, A-B toxins

origins and effects of endotoxins and exotoxins

1) target organs are damaged; heart, muscles, blood cells, intestinal tract show dysfunctions

2) general physiological effects: fever, malaise, aches, shock

process of infection and disease

1) incubation period: time from initial contact with the infectious agent to the appearance of first symptoms, agent is multiplying but damage is insufficient to cause symptoms, several hours to several years

2) prodromal stage: vague feelings of discomfort, nonspecific complaints

3) period of invasion: multiplies at high levels, becomes well-established, more specific signs and symptoms

4) convalescent period: as person begins to respond to the infection, symptoms decline

localized infection

microbes enter the body and remains confined to a specific tissue

systemic infection

infection spreads to several sites and tissue fluids usually in the bloodstream

focal infection

when infectious agent breaks loose from a local infection and is carried to other tissues

mixed infection

several microbes grow simultaneously at the infection site (polymicrobial)

primary infection

initial infection within a given patient

secondary infection

subsequent infection by a different microbe

acute infection

comes on rapidly, severe but short-lived effects

chronic infection

progress and persist over long period of time

patterns of infection

a) localized infection, pathogen is restricted to one specific site

b) systemic infection, pathogen spread through circulation to many sites

c) focal infection, starts and a local infection, but microbe is carried to other sites systemically

d) mixed infection, one site infected with many microbes at the same time

e) primary-secondary infection, an initial infection is complicated by a second one in the same ordifferent location caused by different microbes.

sign

objective evidence of disease as noted by an observer

symptom

subjective evidence of disease as sensed by the patient

inflammation

earliest symptoms of disease as a result of the activation of the body defenses: fever, pain, swelling, edema, granulomas and abscesses (walled-off collections of inflammatory cells and microbes), lymphadenitis (swollen lymph nodes)

leukocytosis

increase in white blood cells

leukopenia

decrease in white blood cells

septemia

microorganisms are multiplying in the blood and present in large numbers

bacteremia

small numbers of bacteria present in blood not necessarily multiplying

viremia

small number of viruses present not necessarily multiplying

asymptomatic

no noticeable or typical symptoms

inapparent (subclinical) infections

although infected, the host doesn't show any signs of disease

typhoid fever ca

Salmonella typhi

typhoid fever s&s

persistent, high fever, headache, constipation, malaise, chills, myalgia, diarrhea uncommon, vomiting not usually severe, confusion, delirium, intestinal perforation, death may occur, tcp: 6-30 days

typhoid fever epidemiology

travelers, sequelae: w/o therapy, may last for 3-4 wks, poverty

typhoid fever transmission

fecal/oral, contaminated food or water, street vended foods

typhoid fever pathogenesis

bacteria invade the small intestine and enter bloodstream temporarily, lyses in the cells, re enter the bloodstream

typhoid fever tx

antibiotic therapy shortens the course of typhoid fever and reduces the risk of death, chloramphenicalty

typhoid fever prevention

oral live vaccine

exit portals

respiratory and salivary: mucus, sputum, nasal drainage, saliva

epithelial cells: skin, scalp

fecal exit, urogenital tract, removal of blood or bleeding

latency

after the initial symptoms in certain chronic diseases, the microbe can periodically become active and produce a recurrent disease, person may or may not shed it during the latent stage

chronic carrier

person with a latent infection who sheds the infectious agent

sequelae

long-term or permanent damage to tissues or organs

epidemiology

study of the frequency and distribution of disease and other health-related factors in defined human populations

reservoir

primary habitat of pathogen in the natural world: human or animal carrier, soil, water, plants

source

individual or object from which an infection is actually acquired

asymptomatic carrier

shows no symptoms

healthcare-associated carrier

contaminated healthcare provider transfers them to other patients

incubation carriers

spread the infectious agent during the incubation period

convalescent carriers

recuperating without symptoms

chronic carrier

individual who shelters the infectious agent for a long period

vector

a live animal (other than human) that transmits an infectious agent from one host to another: fleas, mosquitoes, flies, and ticks, mammals, birds, lower vertebrates

biological vectors

actively participate in a pathogen's life cycle

mechanical vector

not necessary to the life cycle of an infectious agent and merely transports it without being infected

west nile virus ca

Flaviviridae a type of Arbovirus

west nile virus epidemiology

bite of an infected mosquito, mosquitoes become infected when they feed on infected birds

west nile virus s&s

80% asymptomatic, icp: 2-14 days, fever, headache, fatigue, skin rash on the trunk of the body (occasionally), swollen lymph glands (occasionally), eye pain (occasionally)

west nile virus neuroinvasive s&s (west nile encephalitis)

alteration of consciousness, which may be mild and result in lethargy but may progress to confusion or coma, focal neurologic deficits, including limb paralysis and cranial nerve palsies, may be observed, tremors and movement disorders also have been noted

west nile virus pathogenesis

virus replicates within WBC of the skin, WBC's carry virus to lymph nodes where it enters the blood stream, virus can cross the BBB and travel into the CNS infecting brain stem and spinal cord neurons

west nile virus tx and prevention

supportive care, no vaccine, repellant with DEET

zoonosis

infection indigenous to animals naturally transmissible to humans, impossible to eradicate the disease without eradicating the animal reservoir

communicable disease

when an infected host can transmit the infectious agent to another host and establish infection in that host, a highly communicable disease is contagious

non-communicable infectious disease

does not arise through transmission from host to host, occurs primarily when a compromised person is invaded by his or her own microbiota, contact with organism in natural, non-living reservoir

direct contact

physical contact or fine aerosol droplets

indirect contact

passes from infected host tointermediate conveyor andthen to another host• Vehicle - inanimatematerial, food, water,biological products,fomites• Airborne - dropletnuclei, aerosols