First report of the visceral leishmaniasis vector Phlebotomus martini (Diptera: Psychodidae) in Tanzania.

Phlebotomus martini is a known vector of visceral leishmaniasis caused by Leishmania donovani in sub-Saharan Africa. The disease is known to be endemic in areas of north and south Sudan, Kenya, Ethiopia, Uganda, and Somalia but has not been reported from Tanzania. In this report we present the first documented collection of P. martini and P. vansomerenae in Tanzania. Sand flies were collected using standard dry-ice baited CDC light traps (John W. Hock Company, Gainesville, FL) from five sampling sites in the Arusha and Kilimanjaro regions from 14 to 20 July 2010. Phlebotomus martini was collected from all sites and represented 6.6% of the total identified sand flies. Phlebotomus martini ranged from 4.5 to 9.4% of the total identified catch from the four sites in the Kilimanjaro region and 17.9% of the total identified catch at the one collection site in the Arusha region. In addition, one male specimen of the sibling species, Phlebotomus vansomerenae, was found at Chemka Springs in the Kilimanjaro region. These data indicate the presence of an established population(s) of P. martini in northern Tanzania that could support L. donovani transmission in an area with no prior case history of visceral leishmaniasis.

Acute and chronic elevations in serum levels of FSH after unilateral ovariectomy in the cyclic hamster.

During the normal 4-day estrous cycle of the hamster, 12.0 +/- 0.4 (n = 34) ova were shed by the paired ovaries on Day 1. When unilateral ovariectomy (ULO) was performed at 0900 h on any one of the first 3 days of the cycle, approximately the same number of ova were released from the remaining ovary on Day 1 of the ensuing postoperative cycle (compensatory ovulation), except after ULO on Day 4. In view of these results, the principal aim of the present study was to determine if ULO affected acute (24 h postoperative period) and chronic (postoperative cycles) alterations in serum levels of immunoreactive FSH. Multiple bleedings were obtained by cardiac puncture without anesthesia. The acute alteration in FSH levels was first examined at 24-h intervals following ULO at 0930 h on any one day of the cycle, and significant elevations in these levels were found 24 h postoperatively in all but Day-2 hemicastrates. Several experiments were then performed to determine the time-sequence for this 24-h response to ULO. The serum level of FSH was measured at 4-h intervals during the remainder of the cycle in which ULO was done at 0900 h on any one day. The results demonstrated that an acute but transient increase (approximately 100 ng FSH/ml serum) occurred either 7 h or 11 h postoperatively in all the hemicastrates. These transient elevations prior to Day 4 were interpreted to be possible causative factors for the subsequent compensatory ovulation. That they were not the sole cause was evident from the results of another experiment, where compensatory ovulation occurred after ULO at 0030 h on Day 4 (but to a reduced degree; 9.0 +/- 0.6 ova), although serum levels of FSH were not acutely altered. The capability of the remaining ovary to undergo compensatory ovulation after ULO on Day 4 was lost between 0300 h and 0230 h (6.7 +/- 0.8 ova). The serum profile of FSH during the second postoperative cycle after ULO showed a prolonged elevation of FSH levels during the first two days of the cycle compared to the intact estrous cycle. Specifically, the level of FSH gradually declined to 400 ng/ml by 2000 h on Day 1 of the intact (preoperative) cycle but did ont reach this concentration until 2000 h on Day 2 of the postoperative cycle. It is suggested that the prolonged elevated levels of FSH in chronic hemicastrates effect development of a greater number of follicles in the early growth stages in the remaining ovary than the number of follicles per ovary that would otherwise develop in the intact hamster.

The effects of phenobarbital and gonadal steroids on periovulatory serum levels of luteinizing hormone and follicle-stimulating hormone in the hamster.

The occurrence of ovulation and serum levels of LH and FSH (measured by radioimmunoassay) were determined in periovulatory hamsters injected with an ovulation-blocking dose of phenobarbital (Phen) combined with progesterone (P), estradiol-17beta (E2), or testosterone (T). Proestrous hamsters were treated at 1300 h with Phen plus oil, P, P plus E2, E2, T, or a second injection of Phen at 2000 h. Each treatment group was divided into 3 subgroups, each of which was serially bled 4 times at 6 h intervals beginning at 1200, 1400, and 1600 h on proestrus. Phen blocked ovulation on the next morning in all animals, while treatments that included P (1 mg) restored the normal complement of ova in 65-75% of the animals. Neither E2 (1, 10 or 50 mug) nor T (0.1 or 1 mg) overcame the Phen block of ovulation. Control hamsters had peak levels of LH between 1400 and 1800 h and a biphasic release of FSH consisting of a peak at 1600 h on proestrus, a return to basal levels at 2200 h, and a second more sustained surge between 2400 and 0800 h on the morning of estrus. Phen completely depressed the proestrous surge of both gonadotropins but only partially inhibited the second FSH elevation on the morning of estrus. In ovulatory animals, P alone or combined with 1 or 10 mug E2 restored peak LH levels at 1600 h. FSH levels on proestrus in hamsters treated with Phen plus P peaked at 1800 h, while the addition of 1 mug E2 resulted in increased FSH levels at 1600 h; peak levels in both groups were about half of control values. No proestrous increase was detected in ovulatory animals treated with P and 10 mug E2. FSH levels on estrus in hamsters injected with P alone or in combination with E2 were intermediate between those of controls and animals given Phen only. Levels of LH and FSH in animals treated with a single or double dose of Phen or Phen plus E2 or T were not different during the periovulatory period.

Cycloheximide activation of the lordotic response in low-dose, estrogen-treated ovariectomized rats: evidence for modulating inhibitory influences of the limbic system on sexual behavior.

This study tested the effect on intracranially injected cycloheximide (CHX), an inhibitor of protein synthesis, on facilitation of sexual receptivity in ovariectomized rats. The rats received 0.5 microgram estradiol benzoate (EB), s.c. once daily on days 8 through 12 after ovariectomy (OVX). Either CHX (in 0.5 microliter saline) or 0.5 microliter saline was injected into the lateral septum (LS), cortical nucleus (ACO) or medial nucleus of the amygdala or medial preoptic area on day 11 after OVX. The dose of EB was insufficient to facilitate lordotic behavior on day 10 or day 12 after OVX unless CHX was injected into the LS or ACO. Injection of saline did not influence lordosis.

Lesions in the preoptic area suppressed sexual receptivity in ovariectomized rats with estrogen implants in the ventromedial hypothalamus.

The objective of the experiment was to determine if electrolytic ablation of a portion of the preoptic area (POA) influenced the activation of female lordosis behavior by implants of estradiol benzoate in the ventromedial hypothalamus (VMH) of ovariectomized (OVX) rats. Two weeks after ovariectomy, rats received either bilateral electrolytic lesions (2 mA for 10 sec in Experiment 1, or 1 mA for 5 sec in Experiment 2) in the POA, or sham lesions (all procedures except passage of current). On the same day (day 0 of the experiment) thirty-gauge stainless steel cannulae containing crystalline estradiol benzoate were stereotaxically placed bilaterally into the VMH of all the rats. Subsequently, females were tested for the lordosis response to stud males on days 2, 4, 6, 8, and 10 in Experiment 1 or on days 7, 14 and 15 in Experiment 2. All rats received 0.5 mg progesterone (SC) only before the last test. A female was considered sexually receptive if she exhibited a lordosis quotient (LQ) greater than or equal to 10 (LQ = No. lordosis responses/10 mounts by male X 100). The frequencies for sexual receptivity in females with POA lesions were significantly lower than those for control females without lesions in both experiments. Additionally the degree of receptivity (lordosis quotient) was significantly lower on each test day for rats with POA lesions than that for rats without POA lesions. The results imply that the maintenance of the integrity of the POA under this experimental condition was important for the expression of the facilitative influence of the VMH on lordotic responsiveness.

Failure of a synthetic, anti-inflammatory compound to alter the efficiency of the IUD.

Holtzman, female rats with a plastic or copper IUD were maintained on either a dexamethasone solution (9.4 or 28 micrograms/rat/day) in the drinking water or on water alone. Animals were caged with males of proven fertility and subsequently killed at day 14 of pregnancy and the number of implantation sites counted. Both types of IUDs were effective in preventing implantation. Implantation sites were not increased in dexamethasone-treated animals. In addition, proestrous gonadotropin levels and follicular development did not differ between treated and nontreated animals. Thus, the data demonstrate that the efficacy of the IUD is not decreased with the use of anti-inflammatory drugs.

Hypothalamic injection of cycloheximide in the 4-day cyclic rat. Acute suppression of lordotic behavior and ovulation.

The results of serveral studies imply that estrogen can act upon the central nervous system via a protein synthetic step. Our objective was to determine if the intrahypothalamic (preoptic area, POA) injection of cycloheximide (CHX), an inhibitor of protein synthesis, at 17.00 h on diestrus II of the 4-day cycle altered lordotic behavior and (or) ovulation in the intact rat (sexual receptivity to males normally begins on the evening of proestrus as herein defined; ovulation occurs on estrus of the cycle). CHX-treated females were tested for lordotic behavior at 23.00 h on proestrus, then killed at 17.00 h on the following day. None of the CHX-POA rats were receptive to the males and 90% of these rats did not ovulate. Thus, CHX significantly suppressed sex behavior and ovulation in the cyclic rat.