Symptoms, epidemiology, pathophysiology, diagnosis and treatment. For patient education. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/all-animations/microbiology-videos/-/medias/f9bc98ae-8008-40c3-8952-99c6def7864b-infectious-mononucleosis-narrated-animation
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Infectious mononucleosis, or mono, is a very common syndrome characterized by the triad of fever, swollen lymph nodes (lymphadenopathy) – most frequently in the neck, and sore throat with inflamed tonsils (tonsillar pharyngitis). Patients may also present with headache, fatigue, and enlarged spleen upon physical examination. The syndrome can be caused by several different agents, but the most common is Epstein-Barr virus, EBV; and the term “mononucleosis” usually refers to the disease caused by EBV.
EBV is ubiquitous in human. About 95% of all adults have antibodies against EBV, likely from an infection during childhood. Symptomatic infections are most prevalent in older teens and young adults, especially among college students. Infected young children are often asymptomatic or have mild symptoms. Older adults are either immune to the disease thanks to an earlier infection, or have atypical presentations that are misdiagnosed.
EBV is transmitted mainly via infected saliva. The virus is not very contagious, it takes several exposures to high viral loads to acquire EBV. Hence, kissing is the major route of transmission and mono is colloquially known as “the kissing disease”.
The incubation period is typically 3 to 5 weeks. The disease is self-limited and patients usually recover after 2 to 6 weeks, but the virus may remain in the saliva for months. Recovered patients may also shed virus periodically for life without developing symptoms. This is why most people get infected by an asymptomatic person and often cannot recall being exposed to EBV.
After infecting the oral epithelial cells, EBV attacks lymphocytes, in particular B-cells, in the tonsils. Infection then spreads throughout the lymphatic system, causing a massive immune response that is responsible for most of the symptoms. The immune response produces antibodies against EBV, providing lifelong immunity to EBV. At the same time, infection by EBV causes B-cells to proliferate and become antibody-producing plasma cells. Because B-cells are the source of antibodies of all kinds, NON-specific antibodies that do not react to EBV antigens are also produced. These so-called heterophile antibodies may be responsible for the mild thrombocytopenia, generalized rash, and antibiotic-related rash that are occasionally associated with mononucleosis.
As part of the immune defense, cytotoxic T-cells are increased in numbers and activated to kill EBV-infected B-cells. These T-cells have atypical morphology; they are known as Downey cells and are part of the diagnostic workup.
There are 2 antibody tests for mono: monospot test for heterophile antibodies, and EBV-specific antibody test. The monospot test is highly specific, but may give false-negative results in the first week of illness, and has low sensitivity, especially in children. EBV antibody test is performed when monospot test is negative but mono is still suspected.
Mononucleosis is often misdiagnosed as strep throat, and antibiotics may be given inappropriately. Antibiotic treatment can cause a rash to develop and this is often mistaken for antibiotic allergy.
Mononucleosis is self-limited, most patients fully recover after a few weeks, although fatigue may persist for months. Complications are rare but can be severe, sometimes life-threatening.
Treatment is supportive and includes bed rest, hydration, and fever and inflammation reducer. Heavy lifting and active sports must be avoided for a month to prevent splenic rupture. Corticosteroids can be helpful in certain complications, such as impending airway obstruction, but are not usually recommended for uncomplicated disease.

Diagnosing EBV can be done via the heterophile antibody test (“monospot” test), the anti-VCA antibody test, and the anti-EBNA antibody test. The monospot test is neither sensitive nor specific. For more videos and questions, visit – https://www.macrophage.co. Subscribe – https://goo.gl/EMRlRa. Support us on Patreon – https://goo.gl/bhmrgJ.

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(USMLE topics) How the hypothalamus controls body temperature. How fever resets the hypothalamus. Fever versus hyperthermia. This video is available for instant download licensing here https://www.alilamedicalmedia.com/-/galleries/all-animations/immune-and-lymphatic-system-videos/-/medias/1b1d41f8-139e-44a6-8ed2-66127f951376-fever-narrated-animation
Voice by: Ashley Fleming
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Fever, clinically known as pyrexia, is an abnormal increase in body temperature, usually due to an illness. Commonly thought as an undesirable side effect of diseases, fever is actually an effective way the body uses to fight infections. Patients usually recover faster when they allow fever to run its course rather than suppressing it with fever-reducing medications. This is because a higher temperature slows down the growth of most pathogens, as well as boosts the effectiveness of the body’s immune response. It also increases metabolic rates and thereby accelerating tissue repair.
Normally, the hypothalamus keeps the body’s temperature within a narrow range around 37 degrees Celsius, or 98.6 degrees Fahrenheit. The hypothalamus acts like a thermostat. It receives inputs from heat and cold receptors throughout the body, and activates heating or cooling, accordingly. When the body is too hot, the hypothalamus sends instructions for it to cool down, for example, by producing sweat. On the other hand, when temperature drops, the hypothalamus directs the body to preserve and produce heat, mainly via the release of norepinephrine. Norepinephrine increases heat production in brown adipose tissue and induces vasoconstriction to reduce heat loss. In addition, acetylcholine stimulates the muscles to shiver, converting stored chemical energy into heat.
Fever is part of the inflammatory response. When immune cells detect the presence of a pathogen, for example, upon binding to a component of bacterial cell walls, they produce inflammatory cytokines. Some of these cytokines are fever-inducers, or pyrogenic. Pyrogenic cytokines act within the hypothalamus to induce the synthesis of prostaglandin E2, PGE2, the major fever inducer. PGE2 acts on thermoregulatory neurons of the hypothalamus to raise the body’s temperature set point. In other words, PGE2 tricks the hypothalamus into thinking that the body is cold, while in fact the temperature did not change. In response, the hypothalamus instructs the body to actively produce heat to raise body temperature above normal. Fever-reducing medications, such as aspirin and ibuprofen, work by suppressing PGE2 synthesis.
Once infection is cleared, pyrogens are no longer produced and the hypothalamic thermostat is set back to normal temperature. Cooling mechanisms, such as sweating and vasodilation, are activated to cool the body down.
While fever is usually beneficial and need not be treated, precaution should be taken to prevent body temperature from running too high, which may cause confusion, seizures and irreversible damage to the brain.
Finally, it is important to differentiate between fever and hyperthermia, the latter is often caused by extended exposures to extreme heat, or heat stroke. Unlike fever, the body’s temperature set point in hyperthermia is unchanged and the body does not produce the extra heat; its cooling system is simply exhausted and fails to compensate for the excessive external heating. Hyperthermia is always harmful and must be treated with various cooling methods. Fever-reducing medications have no effect on hyperthermia as pyrogens are not involved.
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