Diseases exam 3 Flashcards
Diseases due to streptococcus were first described by
Hippocrates, in the 4th century
When were streptococcal diseases first separated as a disease entity?
The 16th century
Theodor Billroth
First description of a true streptococcal infection was by Theodor Billroth in 1874 and it was associated with wound infections and erysipelas (a skin infection)
How is streptococcus involved in the microbiota?
Many people carry the bacteria on their nasopharynx- does not cause disease in these cases. 5-15% of humans carry S. pyogenes or S. agalactiae, and 20-40% carry S. pneumoniae. This bacteria can be opportunistic pathogens and cause disease
Incidence of respiratory disease due to S. pyogenes
Peaks at 6 years of age and at 13 years of age- most common during late winter and early spring in temperate climates
When are skin infections due to streptococcus most common?
Skin infections are common among preschool age children- most prevalent in late summer and early fall in temperate climates and at all times in tropical climates
S. pyogenes in children
In children, S. pyogenes is associated with invasive disease. It may arise after the child has had varicella. It is also associated with burns or cancer. You become more susceptible to other diseases when you are sick, so skin infections like chicken pox predisposes someone to infect with streptococcus
When does streptococcus cause invasive disease in adults?
In adults, invasive disease is associated with surgical or nonsurgical wounds or underlying medical problems, like diabetes, cirrhosis, underlying peripheral vascular disease, or malignancy
Infectious agent of streptococcus
Streptococcus species are non motile, gram positive coccus bacteria, arranged in chains or pairs
How is streptococcus classified? (3)
- Cell morphology
- Hemolysis ability
- Serologic specificity- cell wall carbohydrates, pili associated proteins, and capsules (group B streptococci)
Clinically important streptococcus species (2)
Streptococcus pneumoniae and streptococcus pyogenes. They are both part of the nasopharynx microbiota that are usually outcompeted by other microorganisms. Some strains of streptococci show a predilection for the respiratory tract, others prefer the skin
How is S. pyogenes generally transmitted?
S. pyigenes is spread by respiratory droplets or contact with fomites. Skin infections often follow minor skin irritations, like insect bites.
Occasional transmission of S. pyogenes occurs due to (3)
- Reports of streptococcal disease traced to rectal carriers
- Food borne- from an infected person preparing the food and transferring bacteria
- Vector borne outbreaks- some vectors carry the bacteria between hosts
Streptococcus enzymes that contribute to disease (6)
- Streptokinase
- DNAse- breaks down DNA
- M protein
- Streptolysin
- Hyaluronidase
- Exotoxins- A, B, and C
M protein
helps the strep bacteria to adhere and is an antiphagocytic factor- prevents the immune system from destroying the bacteria
Streptolysin
a protein that causes hemolysis of red blood cells (hemolytic exotoxin)
Hyaluronidase
an enzyme that can digest host connective tissue and can cause soft tissue necrosis
Exotoxins- A, B, and C
Cause scarlet fever as well as the fever caused by infection. Scarlet fever can lead to rheumatic fever
How is S. pyogenes chemically similar to human cells?
The cytoplasmic membrane of S. pyogenes has antigens similar to those of human cardiac, skeletal, and smooth muscle, heart valve fibroblasts, and neuronal tissues, resulting in a molecular mimicry. Basically causes an autoimmune disease and damages the body’s tissues
Scarlet fever (scarletina)
S. pyogenes is also known to cause strep throat. Bacteria that caused strep throat is infected with a phage- produces an erythrogenic toxin. The phage contains a genetic code for a toxin that attacks red blood cells. The toxin causes inflammation of the skin. The tongue can also appear red. Can still be treated with antibiotics if caught early, but scarlet fever can cause problems later in life if not treated, as well as rheumatic fever
How does previous scarlet fever affect someone’s response to strep in the future?
If a person has had scarlet fever previously, they can develop the rash and symptoms due to a very small amount of the bacteria, since your immune system has produced antibodies against it. Therefore, a person can develop scarlet fever and test negative for strep because there is not enough bacteria to be detected by a test
Erysipelas
known for greater than two thousand years- is caused by hemolytic streptococci. Used to occur often after wounds and surgery. Causes skin infections
Pyoderma and impetigo
caused by Staphylococci, or streptococci alone or in combination- pus producing skin infection
Cellulitis
Extends deeper than erysipelas. The pathogen is only isolated in 25-35% of cases. Develops hours to days after the infection, more slowly than erysipelas. Does not involve the fascia or muscle. Forms a red, hot, swollen lesion that is also painful. Cellulitis is a type of non-necrotizing inflammation, but it may develop into necrotizing fasciitis
How is cellulitis diagnosed? (5)
- Observing symptoms
- Remove aspirates from the advancing edge of cellulitis
- Site of trauma
- Skin biopsies
- Blood
Necrotizing fasciitis
Frequently fatal mixed infection caused by anaerobes and facultative bacteria. Mostly linked to S. pyogenes- thus the term flesh eating bacteria. Radical excision of all necrotic fascia is an essential part of therapy. It is a very acute, toxic infection that causes necrosis of the surrounding tissue. Enters the fascia, muscle, and deeper tissues
Streptococcal toxic shock syndrome
Results from the destruction of tissues during necrotizing fasciitis. Can cause organ damage
How are streptococcal infections diagnosed? (2)
- Serology- fluorescent antibody, direct bacterial agglutination, and ELISA
- Bacterial culturing
Treatment of S. pyogenes
Penicillin is still the drug of choice. However, group D streptococci is resistant to most antibiotics, and group B is resistant to tetracycline
S. pneumoniae vaccines (2)
- Pneumococcal conjugate vaccine- PCV13
- Pneumococcal polysaccharide vaccine- PPSV23
Evolutionary history of herpes simplex virus
HSV-1 infected hominids before their evolutionary split from chimpanzees 6 million years ago. HSV-2 jumped from ancient chimpanzees to ancestors of modern humans. Some infect humans only and some are zoonotic
Herpes Latin meaning
To creep or crawl, described as a spreading skin lesion by Hippocrates
History of HSV
Human transmission was only recognized in 1793. HSV was widely studied in the 1920s-1930s and infects the skin and the nervous system. Varicella-Zoster virus (VZV) has been recorded for many centuries but often was confused with smallpox until the late 18th century. Epstein Barr virus (EBV)- viral particles isolated in 1964. Known for its role in Burkitt’s lymphoma, nasopharyngeal carcinoma, and B cell lymphomas. Cytomegalovirus (CMV) was only isolated recently. It is mostly asymptomatic in the immunocompetent patients- enlarged the infected cells
Which family is HSV part of?
Herpesviridae family
Structure of HSV
Large icosahedral enveloped virus. Linear dsDNA genome that encodes more than 100 genes
Herpes viruses (8)
- HHV-1- Herpes Simplex 1 (HSV-1)
- HHV-2- Herpes simplex 2 (HSV-2)
- HHV-3- Varicella Zoster virus (VZV)
- HHV-4- Epstein Barr virus (EBV)
- HHV-5- Cytomegalovirus (CMV)
- HHV-6A, HHV-6B- Roseolovirus
- HHV-7 Roseolovirus
- HHV-8- Kaposi’s sarcoma associated herpesvirus (KSHV)
Subfamilies of HSV (3)
- Alphaherpesvirinae
- Betaherpesvirinae
- Gammaherpesvirinae
Alphaherpesvirinae
HSV-1, HSV-2, VZV, HHV-8. Variable host range, relatively short reproductive cycle, rapid spread in culture, destruction of infected cells, and capacity to establish latent infection primary but not exclusively in ganglia
Betaherpesvirinae
CMV, HSV-6, HHV-7. Restricted host range, long reproductive cycle, infection progresses slowly in culture, latent in secretory cells, lymphoreticular cells, kidneys, and other tissues
Gammaherpesvirinae
EBV. Host range characteristic of the family or order of the natural host, infects specifically B or T cells, latent virus in lymphoid tissue, may cause lytic infections in some types of epithelioid and fibroblastic cells in lymphocyte, infection may be arrested at prelytic or lytic stage without the production of infectious progeny
Herpes simplex
Human herpesvirus 1 (HSV-1) and 2 (HSV-2). Causes cold sores or fever blisters (vesicles on lips). The virus can be latent and return under stress. Can be found on the skin or genital area. 85% of HSV-2 infections are in the genital area and 90% of HSV-1 infections are oral
Genital herpes
Similar to cold sores but in the genital area. If asymptomatic, someone can still be shedding virus at any time. Preventable by using condoms