Evaluating different pathogens Flashcards
What are virokines and viroceptors, and how do they help viruses evade the immune system?
Virokines: Viral proteins that mimic cytokines, interfering with immune signaling
Viroceptors: Viral proteins that mimic cell receptors, acting as decoys to bind immune molecules & prevent activation
How do bacterial capsules help bacteria evade the immune system?
Capsules cloak bacterial surface proteins, preventing immune recognition
Can be slimy, making it harder for immune cells to engulf & destroy bacteria via phagocytosis
What is viral latency, and which virus is a key example?
Viral latency is when virus shuts off replication & hides in host tissues to avoid immune detection
e.g. Herpesviruses can remain dormant & reactivate during times of stress when immune system is weakened
What are immunoprivileged tissues, and how do pathogens exploit them?
Areas where immune response is limited, allowing pathogens to hide & replicate
E.g. Testes provide sanctuary for some viruses, leading to venereal transmission (e.g. equine viral arteritis)
What is antigenic variation, and why is it important for pathogens?
Mechanism that allows viruses to evade immune detection by changing their surface proteins
Can occur through antigenic drift (gradual changes) or antigenic shift (major genetic reassortment)
What is antigenic drift, and how does it occur?
Small, gradual changes in viral surface proteins due to random mutations
Happens because RNA viruses lack proofreading mechanisms, leading to frequent errors during replication
Results in new viral variants that may escape pre-existing immunity
What is a real-world example of antigenic drift?
Influenza virus undergoes antigenic drift, allowing new seasonal flu strains to emerge
This is why flu vaccines must be updated annually
What is antigenic shift, and how does it occur?
Major genetic reassortment that happens when 2 different strains of virus infect same cell
Their segmented genomes mix, creating new virus with combination of proteins from both parents
How do pathogens directly attack the immune system?
Infect and kill immune cells
Downregulate or inhibit immune effector molecules
Manipulate cell signaling pathways and apoptosis
Why do some pathogens infect immune cells?
Immune cells focus on detecting external infections, making them unaware they are harboring a pathogen
E.g. HIV infects T-helper cells, weakening immune defences
How do pathogens downregulate immune effector molecules?
Switch off cytokine production, preventing immune cell activation
Interfere with immune signaling, reducing body’s response to infection
E.g. some viruses block interferon responses, stopping antiviral defences
How do pathogens manipulate cell signaling and apoptosis?
Inhibiting apoptosis: Some viruses prevent infected cells from self-destructing, allowing longer replication
Promoting apoptosis: Other viruses trigger apoptosis, bursting cells open to release new viral particles
How does Salmonella evade the immune response?
Produces multiple proteins that:
- Block antimicrobial peptides
- Reduce oxidative stress
- Suppress inflammation
- Inhibit lysosome activity, preventing bacterial destruction
Why do some viruses trigger inflammation and cytokine release?
Causes symptoms like coughing & sneezing, increasing viral spread
Inflammation weakens immune system, making host more vulnerable
What is Feline Immunodeficiency Virus (FIV)?
T-lymphotropic retrovirus that primarily affects cats
Causes progressive immune suppression, making cats vulnerable to infections
How does FIV infect host cells?
- Virus enters host cells
- Viral genes & enzymes are released
- Host cells replicate viral components
- New viral particles are released, leading to further infection
Why is FIV difficult to treat with antivirals?
Virus integrates into host DNA, making it hard to target
It mutates frequently, allowing immune evasion
No UK-licensed vaccine currently available
What are the three stages of FIV infection?
Acute Phase:
- Mild illness, fever & CD4+ cell decline
- Neutropenia for up to 9m
Sub-clinical (Latent) Phase:
- Asymptomatic but continuous CD4+ decline
- Virus mutates to evade immune system
Terminal (AIDS-like) Phase:
- Severe immunosuppression → Opportunistic infections develop
What are the key characteristics of the acute phase of FIV?
Mild illness with fever & swollen lymph nodes
Direct infection of CD4+ T cells, causing progressive decline in their numbers
Neutropenia (low neutrophil count) appears 4-8 weeks after exposure & may last for 9 months
What happens during the subacute (asymptomatic) phase of FIV?
Cats appear healthy, this phase may last years or even lifetime
Progressive decline of CD4+ cells continues
Virus mutates to reduce its reliance on CD134, helping it evade immune detection
Why does FIV persist in infected cats despite an immune response?
Immune system reduces viral load, but it can’t eliminate virus
FIV integrates into host’s genome, making it lifelong infection
Mutations allow virus to evade antibody responses & maintain infection
What are the characteristics of the terminal stage (immunosenescence) of FIV?
Severe immunosuppression due to continued CD4+ decline
CD8+ cells outnumber CD4+, disrupting immune function
Opportunistic infections, chronic diseases, neoplasia & neurological disorders appear
Viral load increases due to reduced circulating antibodies
Why are there no typical clinical signs of FIV?
Affected cats often present with persistent infections that they should be able to fight off
Multiple infections may occur at the same time
What are common clinical signs of FIV?
Weight loss
Pyrexia (fever)
Neurological disease
Oral infections (gingivitis, stomatitis)
Enteritis (diarrhea)
Respiratory infections
How is FIV managed?
Supportive care (fluids, antibiotics for secondary infections)
Good nutrition & stress reduction
Treat secondary infections aggressively
How is FIV diagnosed?
PCR testing (detects viral RNA/DNA)
What is the difference between commensal organisms and pathogenic organisms in the reproductive tract?
Commensal organisms: Normally present, don’t invade tissues unless conditions allow
Pathogenic organisms: Have aggressive invasion mechanisms & cause disease
How might commensals help control pathogens?
They compete with pathogens for space & also prime immune system against pathogens
Where are commensal bacteria commonly found in the female reproductive tract?
From most to least bacteria:
Perineum
Vulva
Vestibule
Vagina
Cervix (unless covered with mucus e.g. ruminants/primates)
Uterus (during oestrus)
What are the barriers to entrance of organisms in female reproductive tract?
- Vulva
- Vestibule (Vestibulo-vaginal junction)
- Cervix
Where are commensal bacteria commonly found in the male reproductive tract?
From most to least bacteria:
Preputial skin/lining
Penis
Urethra
(rare in accessory glands, vas deferens or testes)
How does the immune system balance commensal and pathogenic bacteria in the reproductive tract?
Male immunity maintains balance between commensals & pathogens
Female immunity regulates commensals, pathogens, allogenic sperm, and & immunologically distinct fetus
Why might diseases occur in the reproductive tract?
Exposed to pathogenic bacteria or virus
Overgrowth of commensal (but usually requires damage to tissue)
What are the names of infections of different parts of the male reproductive tract?
Preputial skin → Dermatitis
Preputial lining → Posthitis
Penis → Balanitis
Urethra → Urethritis
Prostate → Prostatitis
Testis → Orchitis
What are the names of infections of different parts of the female reproductive tract?
Perineum → Dermatitis/Vulvitis
Vagina → Vaginitis/Vestibulitis
Cervix → Cervicitis
Uterus → Endometritis/Metritis/Pyometra
Uterine tube → Salpingitis (rare)
Ovary → Oophoritis (rare)
Neonates can be infected during birth through birth canal
How can reproductive pathogens be transmitted?
Venereal transmission → Via semen or vaginal secretions
Non-venereal transmission → Other routes (e.g. respiratory tract)
Why is uterine contamination common post-partum?
Cervix remains open & there is damage to endometrium as placenta detaches, allowing commensals or pathogens to enter
Can lead to metritis (deep infection, systemic illness) or endometritis (superficial infection)
Which species are at risk of mating-induced endometritis, and why?
Mare, sow, bitch: Sperm is deposited directly into uterus, increasing bacterial contamination
In healthy animals, bacteria are cleared naturally
In abnormal uterine environments, bacteria persist, leading to infection
Usually female doesn’t become pregnant but rarely infection is controlled & pregnancy occurs but bacterial growth may cause pregnancy loss
What is a common reproductive pathogen causing uterine contamination at mating in mares?
Taylorella (contagious equine metritis (CEM)) causes endometritis
Stallions are asymptomatic carriers
What is a common reproductive pathogen causing uterine contamination at mating in cows?
Bovine venereal campylobacteriosis causes endometritis & sometimes pregnancy loss
Bulls are asymptomatic carriers
How do herpesviruses affect the reproductive tract?
Some herpesviruses are venereally transmitted, causing local lesions in reproductive tract
Others enter via respiratory tract but later infect placenta, leading to pregnancy loss
Recrudescence (reactivation of latent virus) due to pregnancy stress can also lead to placental infection & fetal loss
Which respiratory herpesviruses can infect the reproductive tract in different species?
Horses: EHV-1 → Causes placentitis & abortion
Dogs: CaHV-1 → Causes placentitis & abortion
Cats: FeHV-1 → May cause abortion (rare)
Cattle: BoHV-1 → Causes placentitis & abortion
Which herpesviruses primarily infect the reproductive tract, and what lesions do they cause?
Equine: EHV-3 → Coital exanthema (vesicular lesions on penis & vulva)
Canine: CaHV-1 → Vesicular lesions on penis & vulva
Bovine: BoHV-1 → Infectious pustulovaginitis (vesicular lesions on penis & vulva)
What are the routine reproductive screening tests for horses?
Penile/clitoral swabs for bacterial venereal pathogens (Taylorella, Klebsiella, Pseudomonas)
EVA (Equine Viral Arteritis) serology
Standard vaccination: EHV, EVA
What are the routine reproductive screening tests for dogs?
No routine testing for reproductive pathogens
CaHV-1 vaccination recommended in pregnancy to protect puppies
What are the routine reproductive screening tests for cats?
Toms & Queens: FeLV & FIV serology (before breeding)
Standard vaccination regimes for infectious diseases
What are the routine reproductive screening tests for cattle?
Bulls (non-virgin): Screen for Campylobacter & rarely Trichomonas (sheath washings for culture)
Cows: No routine screening
Brucella surveillance: Regular bulk milk testing, abortion investigations, serology in bulls at semen production centers
Routine serology for BVD, IBR, Leptospirosis
What are the routine reproductive screening tests for sheep?
Rams: Test for Border Disease
Ewes: No routine screening, but empty or aborted ewes tested for Toxoplasma & EAE (Enzootic Abortion of Ewes) via serology
Brucella melitensis screening is performed randomly by DEFRA
What are the routine reproductive screening tests for pigs?
Boars: Serology for PRRS (done weekly in semen production centers), Aujeszky’s Disease, Brucella & Classical Swine Fever
Sows: No routine screening
Routine vaccinations:
- Erysipelas, PPV, Leptospira, PRRS
- E. coli to improve colostral antibodies for piglet protection
