Borrelia recurrentis
a) Adhesion:The human PLG receptor human (plasminogen/Plasmin receptor) present on the endothelium cells are targeted by these organisms.
b) Invasion: the binding of the bacteria to the PLG receptor is associated with another important activity of the production of proteolytic enzymes. They utilize their increased proteolytic capacity to breach tight junctions of endothelium, cross basement membranes, and to initiate pathophysiological processes in the affected organs.
c) Immune escape: It has been recently reported that B. recurrentis expresses a multifunctional surface lipoprotein, termed HcpA, which utilizes the host’s proteins and offers resistance to complement attack and opsonization. The same HcpA is capable of increasing the potential to invade the host’s tissues. Another important feature is antigenic variation.
d) Direct damage: Cause relapsing fever in humans and animals.
e) Indirect damage: Can cause a severe Jarisch-Herxheimer reaction, which is the effect of the faster release of harmful endotoxins in the body than the body can get rid of, during the killing of bacteria by antibiotic treatment. This can even lead to a fatal condition.
Borrelia burgdorferi:
a) Adhesion:
b) Invasion: On the cell surface Borreia burgdorferi expresses different surface proteins, most notably OspA and OspC. These proteins are assumed to play a crucial role in the successful invasion and inhabitance within different organisms.
c) Immune escape: these ticks are capable of producing a protein named Salp15, which works as an immunosuppressive protein. This protein is believed to be involved in the transmission of the bacteria from the vector to the host. And it is probably coating the organism and protecting it from the host antibodies once it's inside the system. Salp15 inhibits T-cell activation too.
Antigenic variation of the surface protein, inactivating the complement system and hiding in the extracellular matrix.
d) Direct damage: Lyme disease is the major disease-associated. Typical symptoms for this disease include fever, headache, fatigue, and a characteristic skin rash called erythema migrans.
e) Indirect damage:May result in facial nerve palsy, pain, sensory loss, or muscle weakness.

Rickettsia prowazekii:
a) Adhesion: the adhesion is presumed to be mediated by the outer membrane proteins. The outer membrane protein OmpA is involved in the process.
b) Penetration: Upon attaching to the host cell membrane, rickettsiae are phagocytosed by the host cell. The rickettsiae induce host cell phagocytosis and enter the cells that normally do not phagocytose particles. Once phagocytosed by the host cell, rickettsiae quickly escape from the phagosome membrane by phospholipase A2 and enter the cytoplasm.
c) Immune escape: it’s capable of escaping from the phagosome by the production of phospholipase A2 enzyme and then multiplies in the cytoplasm.
d) Direct damage: causes epidemic typhus. Signs and symptoms may include • Fever and chills, Headache, Rapid breathing, Body and muscle aches, etc.
e) Indirect damage: Can cause Brill-Zinsser disease to individuals at certain compromised conditions of immune system, old age or illness. There are individuals who remain infected without symptoms for years, these individuals can have Brill-Zinsser disease under aforementioned conditions.
Ehrlichia spp.:
a) Adhesion: Ehrlichiae enters the host cell by receptor-mediated endocytosis. The infectious extracellular forms known as elementary bodies, EB, or dense cored cells, DC attach to the surface of host target cells before entering by endocytosis. This adhesion is mediated by EtpE protein that binds to GPI-anchored protein DNase X.
b) Penetration: By attachment with the cell membrane it’s taken inside the cells by endocytosis. Inside the cell, they develop a membrane-bound vacuole where they survive and replicate. First they differentiate to produce reticulate cells, RB that further divides by binary fission to form large colony called morula. After a few days they again redifferentiate into the elementary bodies (EB) to be released and initiate a new infectious cycle.
c) Immune escape: Ehrlichia escapes the lysosomal degradation by the secretion of ECH_0825, a T4SS (Type IV secretion system) effector, to inhibit apoptosis and ROS production.
Ehrlichia-containing vacuoles are the site for their replication within the cell while replicating they produce T1SS effector proteins (including TRP32, TRP47, TRP120, and Ank200). These effector proteins help them to escape host innate immune responses. In the process of survival in the host cells they also disrupt certain crucial cell-signaling pathways like JAK/STAT to prevent innate immune response.
d) Direct damage: Ehrlichia spp. causes a wide range of symptoms in infected individuals like fever, headache, lethargy, lymphadenopathy, splenomegaly, myalgias and malaise. The greatest distribution of bacteria is observed mainly in tissues containing abundant mononuclear phagocytic cells.
e) Indirect damage: Other manifestations such as thrombocytopenia, leukopenia, and anemia

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