Chapter 2 Understanding infection

Understanding
infection
Definition
 An infection is a host organism’s response to a
pathogen, or disease-causing substance.
 It results when tissue-destroying MO enter and
multiply in the body
 Infection may be minor (flu) or life threatening
(sepsis, meningococcal meningitis,???)
Causes
 I. Viral; have no metabolic capability and need a host
cell to replicate.
 It hide inside the cell and release toxins
 Some viruses surround the host cell and preserve it;
others kill the host cell on contact.
 Bacteria; Pathogenic bacteria contain cell-damaging
proteins that cause infection
 exotoxins—released during cell growth
 endotoxins—released when the bacterial cell wall
decomposes (fever).
 Bacteria may be aerobic/nonaerobic
Causes
 Fungi
 Fungi; large compared to other microorganisms and contain a
true nucleus. Fungi are classified as:
 yeasts; anaerobes,
 Molds; aerobic microorganisms.
 There’s a fungus among us
 Fungi are part of the normal flora, BUT they can overproduce,
especially when the normal flora is compromised.
Ex, vaginal yeast infections can occur with AB treatment
Infections caused by fungi are called mycotic infections because
pathogenic fungi release mycotoxin.
Most of these infections are mild unless they become systemic
 Parasites; uncommon except in hot, moist climates (tapewarm)
Barriers to infection
 Skin
 Secretions from the eyes, nasal passages, prostate
gland, testicles, stomach, and vagina (lysozymes).
 Cilia of the pulmonary airways; sweep foreign
material from the breathing passages.
Trillions of harmless inhabitants
 Normal flora; harmless MO residing on and in the
body.
 They provide useful, protective functions; some help
synthesize vitamin K, which is an important part of
the body’s blood- clotting mechanism.
The infection process
 Infection occurs when the body’s defense mechanisms break
down or when MO virulence or toxin production, override the
defense system.
 Factors facilitate infection occurrence:
 Poor nutrition
Stress
Humidity
Dust
 poor sanitation
Crowded living conditions
Pollution
 Medications (????)
Hospitalization (?????).
 ?????????????
 Enter, attach, and spread
 The pathogen enters the body (???)
 It attaches itself to a cell and releases enzymes that destroy the
cell’s protective membrane.
 It spreads through the bloodstream and lymphatic system,
 finally multiplying and causing infection in the target tissue or
organ.
 Opportunistic infections
Herpes simplex
 A recurrent viral infection, has two types:
 Type 1 primarily affects the skin and mucous membranes
(cold sores/ fever blisters).
 Type 2 primarily affects the genital area, causing painful
clusters of small ulcerations.
 Both types can infect the eyes and other organs in the body,
and can result in localized or generalized infection.
 It’s most prevalent in lower socioeconomic groups
(crowded living conditions).
 The risk of recurrent attacks ;herpes simplex may be
latent for years, outbreaks may be provoked by fever,
menses, stress, heat, cold, lack of sleep, or sun exposure.
Herpes simplex
 Pregnant women should avoid exposure to herpes
simplex; it can cause severe congenital anomalies in
neonates (seizures, mental retardation, blindness, and
deafness).
 Women with herpes simplex type 2 may have an
increased risk of cervical cancer.
 How it happens
 Herpesvirus hominis causes both types of herpes
simplex. Type 1 is transmitted by oral and respiratory
secretions, and type 2 is transmitted by sexual contact.
What to look for (S & Sx)
 Type 1 herpes simplex may cause generalized or localized
infection. Generalized (fever and a sore, red, swollen
throat, submaxillary lymphadenopathy, bad breath, and
anorexia).
 Common sites for vesicles are the tongue, gingiva, and
cheeks, but they may occur anywhere in or around the
mouth.
 With genital herpes simplex, the patient usually complains
first of tingling in the area involved, malaise, dysuria,
dyspareunia (painful intercourse) and, in females,
leucorrhea (white vaginal discharge containing mucus and
pus cells).
 Next, localized, fluid-filled vesicles appear and may last for
weeks.
What tests tell you
 Clinical manifestation
 Biopsy
 CBC
 Treatment
 Symptomatic
 Antiviral
Toxoplasmosis
 Although it usually causes a localized infection, it may
produce a generalized infection in neonates and
immunocopromised clients
 Congenital and deadly
 Congenital toxoplasmosis, characterized by:
 CNS lesions,
 may cause stillbirth or
 serious birth defects.
 It’s transmitted through placenta.
 The severity increased if acquired early in pregnancy.
How it happens
 Intracellular parasite Toxoplasma gondii affects both birds and
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mammals.
It’s transmitted to humans by ingestion of tissue cysts in raw or
undercooked meat or by fecal-oral contamination from infected cats.
Direct transmission can also occur during blood transfusions or organ
transplants.
When tissue cysts are ingested, parasites are released, which quickly
invade and multiply within the GI tract.
• The parasitic cells rupture the invaded host cell and then disseminate
to the CNS, lymphatic tissue, skeletal muscle, myocardium, retina, and
placenta.
As the parasites replicate and invade adjoining cells, cell death and
focal necrosis occur, surrounded by an acute inflammatory
After the cyst reaches maturity, the inflammatory process becomes
undetectable, and the cysts remain latent within the brain until they
rupture.
What to look for
 Mild, localized toxoplasmosis is flu like symptoms
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(malaise, myalgia, headache, fatigue, sore throat, fever)
Severe generalized infection (headache, V, cough, &
dyspnea., high fever 41.1° C, delirium & seizures, rash and
cyanosis.
An infant with congenital toxoplasmosis may have
hydrocephalus or microcephalus, seizures, jaundice,
purpura, and rash.
Other defects; blindness, epilepsy, and mental retardation.
Once infected with toxoplasmosis, the patient may carry the
organism for life. Reactivation of the acute infection can
also occur.
What tellsus
 Clinical manifestation of infection
 Parasite isolation
 Antibodies
 Treatment
 Medications (Sulfadiazine, Pyrimethamine)
 Prevention