2. Pathogenesis, course, epidemiology of infectious diseases, factors influencing the spread of infectious diseases. Flashcards
Course of infectious disease
Incubation time: replicates Seroconversion time: time between infection and immune reaction Course of infection in time Peracute: <6hrs Acute: few days Subacute: few weeks Chronic: >4 weeks to several years
Outcome of disease
Complete recovery
Partial recovery: following chronic diseases
- Residual symptoms: pneumonia can give abscess in lung or even atelectasis, arthritis, infertility
Death
Carry and shed the agent
- Temporary/long lasting (even in case of immunity, ex. TB, Brucellosis)
- Also in case of asymptomatic infection
- Maintains chain of infection
- Local infection
(tetanus, papillomatosis)
Lesions at place of entry only
Entry - colonization - replication - damage (+ shedding)
- Infection of different organs
(rabies)
Localized - lesions in one organ
Entry, getting into target organ, manifestation - colonization - replication - local damage
- Generalized infections
(anthrax, ASF)
Lesions in more organs
Incubation - infection - colonization - start of replication
- Generalization
Spreading via blood, lymphatic vessels or perineural (rabies)
Viremia, bacteremia, septicemia
In the organ the agent will replicate and damage the host with toxins, EC enzymes etc.
Manifestation of a disease
CS, lesions (virulence factors), intracanicular spread (chronic diseases)
Fetus: (fetopathic agents) embryonic death, resorption, abortion, teratogenic, decreased resistance (born with infection, not viable), tolerated infections
Course of infectious diseases caused by viruses
Replication at place of entry and regional LN (exceptions: e.g. rotavirus (small int) and papillomatosis)
Localization by macrophages: can enter the blood - frequently cell bound viremia
Replication in infected macrophages, lymphocytes, blood (viremia)
Replication in lymphoid cells (immune suppression, activity of lymphocytes and macrophages will be slightly suppressed, damage of blood vessels: hemorrhages will be present (PM)
CS:
Secondary replication in tissues: damage of cells
Reactive inflammation, start of immune allergic reactions - makes CS worse
Asymptomatic infection
Inapparent (subclinical) infection: resistance of host can limit the activation of agent - cannot damage host severely
Difficult to diagnose BUT SHEDDING
Persistent, latent, tolerated infection
Persistent infection
Virus
Agent present in lymphoid cells
Antibodies, immune complexes, allergic processes, tumor transformation
e.g. ASF, Mareks
Latent infection
Virus
ø complete viral replication
integration of the virus genome into the genome of the cell of hosts
Stress can trigger the activation of the infection so it appears to come out of nowhere - NO SHEDDING
e.g. HERPES
Tolerated infection
Virus
Infection before fetal immune recognition
Pregnant animal has disease and agents gets into fetus before immune competence - the agent is regarded as part of the immune system - no response, hard to diagnose STILL SHEDDING
e.g. BVD
Epidemiology of infectious diseases, data analysis
Susceptible species, vectors Characteristics of populations Spreading (geography, time) Etiology, predisposing factors Epi follow up Analysis --> diagnostic work
Dead end host
Has CS but does not shed e.g. WNV, horse and human
Soil infection examples
Bacillus anthracis spores, tetanus spores