An infectious disease occurs when a pathogenic organism causes inflammation or organ dysfunction. This may be caused directly by the virus itself, as when the etiologic agent multiplies in the coordinator, or indirectly as a result from the host’s inflammatory response. Numerous infections are subclinical, not producing any obvious manifestations of illness.
To cause overt virus, all microorganisms should go via the following stages: The microorganism should (1) come across the host, (2) gain entry into the coordinator, (3) multiply and spread from the website of entry, and (4) trigger host tissue injury, either directly (eg, cytotoxins) or indirectly (host inflammatory response).
The severity of virus ranges from asymptomatic to life threatening, and the course may be characterized as acute, subacute, or chronic. Regardless of whether virus is subclinical or overt, the outcome is either (1) resolution (eg, eradication from the infecting pathogen), (a couple of) continual active virus (eg, HIV or hepatitis), (three) prolonged asymptomatic excretion of the agent (eg, carrier state with Salmonella typhi), (4) latency from the agent within coordinator tissues (eg, latent tuberculosis), or (5) coordinator death from virus.
Except for congenital infections (acquired in utero) caused by agents such as rubella virus, T pallidum, and cytomegalovirus, human beings first come across microorganisms at birth. During parturition, the newborn comes into contact with microorganisms existing within the mother’s vaginal canal and on her skin. Most from the bacteria the newborn encounters don’t trigger harm, and for those that might cause virus, the newborn usually has passive immunity via antibodies acquired from the mother in utero.
For example, neonates are protected against infection with H influenzae by maternal antibodies for the very first 6 months of existence until passive immunity wanes and also the chance of infection with this bacterium increases. On the other hand, newborns whose mothers are vaginally colonized with group B streptococci are at increased risk in the perinatal period for serious infections such as sepsis or meningitis with this organism.
Direct entry to the coordinator (ie, bypassing the usual chemical and physical barriers) occurs via penetration. This might occur when (1) an insect vector directly inoculates the infectious agent to the host (mosquitoes transmitting malaria), (2) bacteria gain direct access to coordinator tissues through loss of integrity from the skin or mucous membranes (trauma or surgical wounds), or (three) microbes gain access via instruments or catheters that permit communication between generally sterile websites and the outside world (eg, indwelling venous catheters).
Ingression occurs when an infectious agent enters the host via an orifice contiguous with the external environment. This primarily involves inhalation of infectious aerosolized droplets (M tuberculosis ) or ingestion of contaminated foods (salmonella, hepatitis A virus). Other infectious agents directly infect mucous membranes or cross the epithelial surface to cause virus.
This commonly happens in sexually transmitted diseases. For example, HIV can cross vaginal mucous membranes by penetration of virus-laden macrophages from semen. Right after the initial come across with the host, the infectious agent should successfully multiply at the site of entry.
The procedure whereby the newly introduced microorganism successfully competes with normal flora and is able to multiply is termed colonization (eg, pneumococci colonizing the upper respiratory tract). When the microorganism multiplies at a usually sterile site, it is termed virus (eg, pneumococci multiplying within the alveoli, causing pneumonia).
Elements that facilitate the multiplication and spread of infection include inoculum size (the quantity of infectious organisms released), coordinator anatomic factors (eg, impaired ciliary function in children with cystic fibrosis), availability of nutrients for the microbe, physicochemical factors (eg, gastric pH), microbial virulence elements, and microbial sanctuary (eg, abscesses).
An abscess is a special case by which the coordinator has contained the virus but is unable to eradicate it, and these localized infections generally need surgical drainage. Once released, infections can spread along the epidermis (impetigo), along the dermis (erysipelas), along subcutaneous tissues (cellulitis), along fascial planes (necrotizing fasciitis), into muscle tissue (myositis), along veins (suppurative thrombophlebitis), into the blood (bacteremia, fungemia, viremia, etc), along lymphatics (lymphangitis), and into organs (eg, pneumonia, brain abscesses, hepatitis).
Infections cause direct injury to the coordinator through a variety of mechanisms. If organisms are existing in sufficient numbers and are of adequate size, mechanical obstruction can happen (eg, children with roundworm GI infections may present with bowel obstruction).
More commonly, pathogens trigger an intense secondary inflammatory response, which may outcome in life-threatening complications (eg, kids with H influenzae epiglottitis might existing with mechanical airway obstruction secondary to intense soft tissue swelling of the epiglottis).
Some bacteria produce neurotoxins that affect host cell metabolism rather than directly producing cell harm (eg, tetanus toxin antagonizes inhibitory neurons, producing unopposed motor neuron stimulation, manifested clinically as sustained muscle rigidity). Host cell death can occur by a variety of mechanisms. Shigella produces a cytotoxin that causes death of big intestine enterocytes, resulting in the clinical syndrome of dysentery.
Poliovirus-induced cell lysis of the anterior horn cells from the spinal cord leads to flaccid paralysis. Gram-negative bacterial endotoxin can initiate a cascade of cytokine release, resulting in sepsis syndrome and septic shock. The time course of an infection could be characterized as acute, subacute, or continual, and its severity may vary from asymptomatic to existence threatening.
Numerous infections that begin as mild and very easily treatable conditions readily progress without having prompt treatment. Small, seemingly insignificant skin abrasions superinfected with toxic shock syndrome toxin (TSST-1)-producing S aureus can outcome in fulminant infection and death. Even indolent infections, such as infective endocarditis resulting from Streptococcus viridans, can be fatal unless they’re recognized and appropriately treated.
There are three potential outcomes of infection: recovery, chronic virus, and death. Most infections resolve, possibly spontaneously (eg, rhinovirus, the leading trigger from the common cold) or with medical therapy (eg, right after remedy of streptococcal pharyngitis with penicillin). Continual infections may be either saprophytic, by which situation the organism does not adversely affect the health of the coordinator; or parasitic, producing tissue harm towards the coordinator.
An instance from the former is Salmonella typhi, which might be harbored asymptomatically within the gallbladder of about 2% of individuals right after acute infection. Chronic infection with the hepatitis B virus might be either saprophytic, in which situation the human coordinator is infectious for that virus but has no clinical evidence of liver harm, or parasitic, with progressive liver damage and cirrhosis.
A final form of continual virus is tissue latency. Varicella-zoster virus, the agent causing chickenpox, survives in the dorsal root ganglia, with reactivation causing a dermatomal eruption with vesicles or shallow ulcerations, commonly known as shingles. When the ability of the immune system to control possibly the acute or the chronic infection is exceeded, the virus might result in coordinator death.
A unifying theme is that all infectious agents, regardless of specific mechanisms, must successfully reproduce and evade host defense mechanisms. This knowledge helps the physician to avoid infections (eg, vaccinate against influenza virus); when virus occurs, to treat and cure (eg, antibiotics for E coli urinary tract infection); and when virus cannot be cured, to avoid further transmission, recurrence, or reactivation (eg, barrier protection to decrease the sexual spread of genital herpes simplex infection).