MICR EXAM PATHOGEN

Spell the name of the pathogen

Borrelia burgdorferi

what does pathogen cause?

Lyme disease

Cases of lyme disease are increasing because

climate change is expanding the range of the tick that carries it. 

what type of tick carries borrelia burgdorferi

Ixodes ticks

what kind of interacton does Borrelia burgdorferi have with host?

obligate parasite

how does Borrelia burgdorferi infect ixodes ticks?

ticks feed on small mammals infected with Borrelia burgdorferi, it then enters the tick and the tick can now spread to the next thing the tick feeds on

ticks feed and reproduce on deer, do deer get Borrelia burgdorferi?

no, deer are immune to Borrelia burgdorferi

describe ideal temp, oxygen and pH for Borrelia burgdorferi

only ever lives inside warm hosts or ticks, it prefers 37°C, low oxygen, and neutral pH — conditions that mirror the mammalian body.

is Borrelia burgdorferi an obligate parasite?

yes, relies entirely on its host to supply them. This metabolic dependence is a direct consequence of living as a parasite for so long.

KPCOFGS?

• Kingdom: Bacteria

• Phylum: Spirochaetes

• Class: Spirochaetia

• Order: Spirochaetales

• Family: Borreliaceae

• Genus: Borrelia

• Species: Borrelia burgdorferi

gram?

negative

morphology

spirochete

what kind of flagella? why it matters?

periplasmic flagella/ endoflagella- instead of sticking out from the cell surface like normal bacterial flagella, they run inside the cell, in the space between the inner and outer membranes. 

hides the flagella from the immune system — flagellin is a protein the immune system is very good at detecting.

internal flagella act like a corkscrew that lets the cell drill through thick, gel-like tissues (like joint fluid and connective tissue) that would stop a normal bacterium in its tracks. Both features directly help it invade and spread in the body. 

how are humans infected with Borrelia burgdorferi?

tick bit: the tick needs to be attached for over 24 hours before it can transmit the bacteria, because the bacteria need time to travel from the tick's gut to its saliva- removing tick quickly actually prevents infection.

(Nymphal ticks (the juvenile stage) cause most human cases because they are tiny — about the size of a poppy seed — and people often don't notice them)

humans are dead end hosts why?

we dont continue to spread the Borrelia burgdorferi (often dont give it back to another tick vector)

what does lymes disease look like in body? how does it occur in stages?

Within days of the tick bite, bacteria multiply at the skin entry point. A rash often appears and it expands outward from the bite site in a “bullseye shape.” Flu-like symptoms accompany this. At this point the bacteria are still localized and antibiotics can kill the infection.

If untreated,Borrelia burgdorferi enters the bloodstream and spreads — usually over weeks to a few months. It can cross into the nervous system (causing facial palsy or meningitis), reach the heart (causing a partial or complete heart block), and seed distant skin sites causing multiple rashes.

if still untreated, bacteria will have embedded in collagen-rich tissues particularly large joints like the knee and trigger a persistent, aggressive inflammatory response. Lyme arthritis is the hallmark: hot, swollen joints. Neurological symptoms like cognitive fog and fatigue also emerge. Crucially, much of the damage in this stage is the body's own prolonged inflammatory immune response harms the joints and nerves- often even after Borrelia burgdorferi clears immune response to debris still causes issues

does Borrelia burgdorferi make toxins?

B. burgdorferi makes no toxins- does not inject anything into your cells, and does not replicate inside your cells. All the damage comes from your own immune system's inflammatory response to the bacteria being there, combined with the bacteria's ability to persist and spread by evading immune response. 

Virulence factors  

Since there are no toxins, all virulence comes from surface proteins that switch on and off depending on whether the bacteria are in a tick or a mammal. The first key protein is OspC, which turns on when the tick starts feeding. OspC helps the bacteria move from the tick gut to the saliva for transmission, and once inside the mammal, it grabs onto a tick saliva protein called Salp15 that suppresses the local immune response — essentially using the tick's own immune-dampening molecule as a shield. Once the host's adaptive immune system starts making antibodies against OspC, the bacteria switch it off. The bacteria then turn on VlsE, which is their main long-term survival tool. VlsE is a surface protein that constantly reshuffles its own gene sequence, generating new surface variants that the host's antibodies don't recognize. By the time the immune system makes antibodies to one version, VlsE has already changed. This is called antigenic variation and is why the bacterium can persist for months to years in an immunocompetent host. To get into tissues, the bacteria use BBK32, a surface protein that grabs onto fibronectin (a protein in blood vessel walls and connective tissue). This lets them latch onto the inside of blood vessels even against blood flow, then squeeze through into surrounding tissue. Finally, to avoid being killed by complement, the bacteria use their CRASP/Erp family proteins to recruit host complement-inhibitory proteins (Factor H and FHL-1) onto their own surface — essentially borrowing the host's own off-switch for complement to protect themselves. 

Treatment + vaccines  

Lyme disease is treatable with antibiotics and most people recover fully if treated early. The go-to antibiotic is oral doxycycline.For severe cases involving the brain or heart, IV antibiotics can be used. Unlike many other bacteria, B. burgdorferi has not developed significant antibiotic resistance. 

A major unresolved problem is Post-Treatment Lyme Disease Syndrome (PTLDS) — about 10–20% of treated patients still feel fatigued, achy, and cognitively foggy for months after finishing antibiotics. Nobody fully knows why. Possibilities include ongoing inflammation, an autoimmune response that got triggered, or bacterial forms (like round bodies or biofilms) that antibiotics don't fully clear. Importantly, giving more or longer antibiotics does not help and is not recommended. 

There is no currently approved human vaccine. The only one that ever existed, targeted OspA, but, was pulled from the US market in 2002 because of low sales and unproven concerns it might trigger arthritis.

research

The biggest active research area is mRNA Lyme vaccines — using the same lipid nanoparticle technology that made the COVID-19 vaccines work. A 2025 study from Institut Pasteur and Sanofi showed that an mRNA vaccine targeting OspA produced stronger antibody responses than a traditional protein-based vaccine and fully protected mice from tick-transmitted infection. Moderna has two mRNA Lyme vaccine candidates (mRNA-1975 and mRNA-1982) currently in Phase 1/2 human clinical trials. 

A different approach called "Lyme PrEP" skips the immune system entirely. Instead of a vaccine, it involves injecting a pre-made monoclonal antibody against OspA once a year before tick season. When an infected tick bites and feeds, it takes up the antibody with the blood meal — the antibody then kills the bacteria inside the tick's gut before they can ever be transmitted. It's essentially seasonal pre-exposure prophylaxis, similar in concept to PrEP for HIV. 

describe complex geneome

it has an unusually complex genome — specifically, it carries the largest plasmid complement of any characterized bacterium, and most of its disease-causing genes are on those plasmids rather than its main chromosome. Second, it is exceptionally good at hiding from the immune system by constantly swapping out the proteins on its surface so the immune system can never get a lasting grip on it. These two features together explain why Lyme disease can become chronic and hard to clear.