Fig 1.
The study design.
Fig 2.
Changes in Loa mf loads a different time points.
a. Untreated animals. b. Following ivermectin treatment.
Table 1.
Blood peripheral mf loads before and after different treatments.
Fig 3.
Changes in Loa mf loads with different treatment regimes.
: ivermectin alone (IVM), ivermectin and aspirin (IVM+ASA), and ivermectin and prednisone (IVM+PSE).
Fig 4.
Variations in clinical presentations after ivermectin treatment (A = temperature; B = respiratory rate; C = pulse rate).
Fig 5.
The typical behavioral response after treatment: Depression and reluctance to participate in normal activities.
Fig 6.
Dermatological responses in baboons after treatment.
Score for rashes and pruritus in baboons following ivermectin treatment (Ranges used = 0: Normal/Absent/no alteration, 1–5: Mild, 6–10: Moderate, 11–15: Severe and 16–20: Unbearable).
Fig 7.
Macroscopic changes following ivermectin treatment.
A. Petechial haemorrhages in the central nervous system, B. Cardiac muscle section showing petechial haemorrhage, C. Petechial haemorrhages in the lungs, D. Haemorrhagic lymph nodes in the omentum, E. Adult worm lesion present in the deep subcutaneous tissues, and F. Newly formed splenic tissues approximately 18 months after splenectomy.
Fig 8.
Distribution of L. loa mf in the tissues of different organs in the four experimental groups: Control animals, animals given ivermectin alone, animals given ivermectin and aspirin animals, and animals given ivermectin and prednisone.
Fig 9.
Microscopic lesions present in the untreated and in the first 72 hours after treatment.
A. Microfilariae in dermal vessels. B. Eosinophil accumulation in the tissues, a typical response in the first 24 hours, C. Blood vessel free of mf- many normal vessels can also be seen free of mf in this phase, D. Accumulation of mf in the lymphoid tissues, an event that is common within the first 2–3 days, E. Fibrin deposition (red) on the walls of a cerebral vessel. F. Area of mf degeneration and eosinophil accumulation/degranulation in a lymph node.
Fig 10.
Microscopic lesions present in the treated animals more than 72 hours after treatment.
A. Adult L. loa worm in connective tissue beneath the skin. B. Blocked CNS vessel comprised of eosinophils, fibrin, macrophages and parasite debris. C. Blocked CNS vessels with associated damage (vacuolation of the parenchyma). D. Intact microfilariae caught in a cellular intravascular mass in the CNS, E. A degenerating mf in a capillary of the CNS and surrounded by fibrin. F. Area of vascular and parenchymal damage in the CNS predominately filled with macrophages and eosinophils.
Table 2.
Presence and extent of histo-pathological changes in different organs (No. of animals per group).
Table 3.
Distribution of lesions between the different treatment groups (No. animals per group).
Fig 11.
Potential pathogenesis of Loa encephalopathy following the ivermectin treatment of Loa hyper-microfilaraemic individuals.